Medical Science Publication No. 4, Volume 1
SHOCK
A STUDY OF THE KOREAN BATTLE CASUALTY*
JOHN M. HOWARD, M.D.
To appreciate shock following injury is to appreciate the entire fieldof trauma: the wounding agents, the nature of the injuries, the body'sresponse to injury, the characteristics of the resuscitative agents, theeffectiveness of the resuscitative methods, and the sequelae of injury,for all are entwined in the clinical syndromes found in the wounded soldier.As we learn more about the nature of injury and the body's response toinjury, we shall, as so fittingly suggested by Green and Stoner, discardthe term shock and speak of the specific injury and the specific resultantdeficiency and response. We can almost justify such a step now. The valuein retaining such an all-inclusive term is only to focus attention on theserious deficiency of the circulatory system. There is no common causeof hypotension following injury and therefore no common therapy. A woundof the central nervous system may produce hypotension by injury to thesympathetic nervous system. An injury to the heart or pericardium may producehypotension due to a primary deficiency in cardiac output. An open chestwound may produce hypotension due presumably to a loss of the thoracicpump mechanism and so a decrease in return of blood to the right side ofthe heart with a resultant decrease in cardiac output. These are specificwounds causing specific deficiencies and requiring specific therapy. Toclass these patients together under any single diagnosis or plan of therapywill result in added fatalities.
Hypotension and shock are therefore no more specific than fever or jaundice.Like the latter terms, however, they serve to focus attention on the gravityof the situation in the individual patient. Although hypotension may havemany causes, the chief factor in most casualties, as was pointed out bytbe Board for the Study of the Severely Wounded, is a deficiency in bloodvolume. It is this group of patients with injuries primarily of the abdomenand extremities with whom we are chiefly concerned.
*Presented 21 April1954, to the Course on Recent Advances in Medicine and Surgery, Army MedicalService Graduate School, Walter Reed Army Medical Center, Washington, D.C.
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The present concept of shock, as further developed in our Korean studies,is based on our knowledge of the nature of the injury and the body's responseto the injury. Such knowledge may be summarized as follows:
1. The battle wound is dynamic. The battle wound results in a defectwhich produces a continuing deleterious effect. This continuing deleteriouseffect must be minimized by operative débridement.
2. Following injury the body responds to correct the defects. This isa continuing response of every organ and system which has been studied.This response may be life-saving.
3. Anesthesia blocks part of the patient's response and therefore, atleast for the moment, furthers the injury.
The thoughts expressed grew out of the many informal conversations heldaround the litters of the wounded at the 46th Surgical Hospital and aroundthe laboratory of the Surgical Research Team in Korea. Many of the expressionsare thus not original with the speaker and much of the work mentioned isthe work of his colleagues.
With severe injury there is a response of every part of the body tocompensate for, and reverse or heal the injury. This compensatory mechanism,like life itself, is an interdependent mechanism, dependent upon the circulationof blood from one capillary bed to another. It is a continuing response.One element of the injury is blood loss. When blood loss is of sufficientdegree, an inadequate circulation results. Hypotension is one manifestation.This state of circulatory insufficiency damages the various organs takingpart in the compensatory effort. Circulatory insufficiency, produced primarilyby blood loss, therefore furthers the injury by destroying the defensemechanism.
Shock might therefore be defined as the clinical picture of an inadequatecirculation following trauma. It is due initially to an inadequate circulatingblood volume.
What is the background to wound trauma? A massive wound includes thefollowing elements:
1. Tissue destruction.
2. Blood loss.
3. Bacterial contamination.
4. Mechanical defects.
These are the four wounding elements. A fifth which may ultimately proveof importance is the direct transmission of energy from the missile tothe entire body, depicted only locally as tissue destruction. A functionalaberration, quite distal to the missile, may prove to result from the directtransmission of energy just as with an elec-
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trical shock. All of these elements of the wound produce a deleteriouseffect, the summation of which Churchill has termed wound shock.
Tissue destruction produces a dynamic wound. It is not an injury whichoccurs for the moment. As Beecher described, it continues to exert itsdeleterious effect. Blood is lost externally and into the injured areas.Albumin, water and electrolytes are extruded. Products of tissue breakdownare absorbed as are the toxins of bacterial action. Thus there is an exchangeof substances by the circulation at the site of the undébrided woundto the net disadvantage of the body (fig.1).
With a severe injury, the body responds in toto. Every system,every organ and presumably every cell in the body responds to severe trauma.
Among the responses we recognize are the following; there is much overlap,but the following list indicates a way of thinking:
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A. The emotional response of fear.
B. Response to tissue destruction.
1. Pain.
2. Inflammation.
3. "Metabolic débridement" (internal débridement)of the wound.
4. Tissue slough (external (débridement).
5. Wound healing.
C. Response to blood loss.
1. Response of the autonomic nervous system.
2. Adrenal cortical response.
3. Renal vasoconstriction.
4. Increased production of clotting factors.
5. Regeneration of red blood cells and proteins.
D. Response to bacterial contamination.
1. Leukocytic response.
2. Antibody formation.
E. Response to mechanical defects-circulatory and respiratory changesfollowing increased intracranial pressure, respiratory obstruction, cardiactamponade, sucking chest wound, etc.
F. Paralytic ileus.
These responses are part of the compensatory mechanisms. Most of themare a response to hemorrhage and tissue destruction.
As a result of some of these responses, compensation of the circulationmay result, but if the initial trauma is too great, or is repeated, andthe resultant blood loss is too great, peripheral vascular inadequacy results.This does not imply a decompensation of the peripheral vascular mechanism.The autonomic system, heart and peripheral vascular bed may be functioningmaximally. The injury and blood loss were simply so great that the compensatorymechanism could not maintain an adequate circulation. Hypotension results.
Most of the studies of shock have centered around the loss of bloodand certainly this is the heart of the problem. Our studies confirmed theobservation of others that with a rapid loss of 25 percent of the bloodvolume, hypotension develops. Up to this point, the heart and autonomicnervous system, by increased cardiac rate and vasoconstriction, can compensatefor the loss to maintain a normal pressure. After the rapid loss of 25percent (about 1,200 cc.) hypotension develops and after a rapid loss of40 percent (2,000 cc.) hypotension is profound. Now, as seen at the forwardsurgical hospital, this hypotension can invariably be reversed before anesthesiaif the central nervous system is intact and if hemorrhage can be stopped.In over 4,000 casualties there was no exception to this statement. At anaverage time of 3.5 hours after injury and before anesthesia, every casualtycould have
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his blood pressure restored to a normal level provided there was noinjury to his central nervous system and provided hemorrhage could be controlled.To repeat, in the resuscitation of 4,000 battle casualties at an averagetime of 3.5 hours after injury, irreversible shock was not recognized priorto anesthesia provided hemorrhage could be controlled and there was noinjury to the central nervous system. Continued hypotension, at this earlytime was, therefore, the result of continued hemorrhage or inadequate transfusion.Anesthesia blocks part of the compensatory mechanism and may convert thecompensated circulatory system to that of a profound shock. Furthermore,after anesthesia, shock may become extremely, even fatally, resistant totransfusion therapy.
The purpose of the circulatory system is to circulate substances fromone capillary bed to another-from lungs to limb, from liver to brain, frombowel to liver, to heart, etc. Circulatory failure is, therefore, a failureof capillary circulation. This failure is brought on by a reduction inthe circulating blood volume and I emphasize volume. If the volumeis suddenly reduced 50 percent, circulatory failure is profound with theblood pressure unobtainable (fig. 2). Under these conditions, total volume,plasma volume and red cell mass are each reduced by 50 percent. Death isimminent. Now, if the 2,500 cc. loss is replaced by dextran in such anamount that the total blood volume is restored, the red cell mass remainsat the low
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volume of 1,125 cc. so that the hematocrit drops to 22.5 percent. Thered cell mass, therefore, has not been changed from that of the severeshock state. Blood volume has been restored, the patient has now responded,his blood pressure is normal, his pulse rate somewhat fast but slower thanbefore therapy, and the man has now compensated (fig. 3). The reserve istherefore far greater in red cell mass percentagewise, than in blood volume.Circulating blood volume and capillary flow or pressure are therefore theimportant elements. This fact permitted the use of plasma volume expandersacross the front and the response was satisfactory. This was, of course,a compromise based on the relative non-accessibility of whole blood inthe front lines.
The value of whole blood transfusions was appreciated in World War II.In Korea, the helicopter and the supply of whole blood available combinedto permit the treatment of many casualties who would previously have diedin transit or been considered hopeless. We literally poured blood intothese men. Often the question was raised as to whether too much blood wasused. We knew from experience that, if transfusion was slowed, hypotensionand death resulted. Captain Prentice has summarized the blood volume studieswhich unequivocally demonstrated the justification for massive transfusionsin most of the severely injured men. This experience with massive transfusionswas unique.
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The following three tables (tables 1, 2, and 3) demonstrate some ofthe practical observations. Table 1 summarizes the experience with 30 consecutivepatients studied whose blood pressure at the time of admission to the hospitalwas zero as measured clinically. Nine patients required less than 15 pintsof blood. There was no fatality. Twenty-one patients required over 15 pintsand the mortality was 52 percent. In the latter group, the mortality inthe seven patients with wounds limited to the abdomen was 100 percent incontradistinction to a mortality of only 12.5 percent of the eight casualtieswith wounds of the extremities. One of the implications of the latter comparisonis the difficulty in controlling intra-abdominal hemorrhage. Greater immediatedividends will accrue from studies on methods of controlling hemorrhagethan from studies on the mechanisms of late shock. Another implicationfrom this study is that the amount of blood required for resuscitationis a better index of prognosis than is the blood pressure at the time ofadmission.
Table 1. Resuscitation of Battle Casualties-AdmissionBlood Pressure Unobtainable
| Total | Receiving 15 or more pints of blood | Receiving less than 15 pints of blood | |||||
Number | Mortality (percent) | Number | Number died | Mortality (percent) | Number | Number died | Mortality (percent) | |
Abdominal only | 10 | 70 | 7 | 7 | 100 | 3 | 0 | 0 |
Abdominal and extremity |
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Extremity only | 14 | 7 | 8 | 1 | 12. 5 | 6 | 0 | 0 |
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Table 2 summarizes the experience with 60 casualties (regardless ofadmission blood pressure) who required 15 or more pints of blood on theday of admission. Again continued hemorrhage was recognized as a majorfactor accounting for 10 deaths and Captain Prentice has data to indicatethat many of the others died of blood volume deficiency in spite of massivetransfusion and in spite of apparent hemostasis. Again, the sharp differenceis noted between the mortality in the patients with abdominal and extremitywounds.
Finally (table 3), it was in this group who required massive transfusionthat post-traumatic renal insufficiency developed. This complication isa direct or indirect result of the magnitude of the wound and the severityof the shock. Post-traumatic renal insufficiency cannot be predicted byevaluating the magnitude of the wounds or the
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Table 2. Resuscitation of Battle Casualties-PatientsRequiring 15 or More Pints of Blood in First 24 Hours
| Total | Number dying of continued hemorrhage | Mortality excluding continued hemorrhage (percent) | ||
Number | Number died | Mortality (percent) | |||
Abdomen | 16 | 13 | 81 | 7 | 67 |
Abdomen and extremities | 20 | 10 | 50 | 2 | 42 |
Extremities | 21 | 2 | 9. 5 | 0 | 9. 5 |
Chest | 3 | 2 | 67 | 1 | 50 |
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Table 3. Resuscitation of Battle Casualties-PatientsRequiring 15 or More Pints of Blood in First 24 Hours, Incidence of RenalFailure
Injury | Number living 3 days or longer | Anuria (percent) | Oliguria (percent) | Non-oliguric azotemia (percent) |
Abdomen | 9 | 22 | 11 | 11 |
Abdomen and extremity | 14 | 28 | 0 | 7 |
Extremity | 19 | 0 | 11 | 22 |
Chest | 1 | 0 | 0 | 0 |
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Incidence of clinically significant renal failure=35 percent.
severity of the hypotension at the time of admission. It can best bepredicted by the response to transfusion. The hypotensive patient withserious wounds, whose blood pressure responds sluggishly to transfusionin the face of apparent hemostasis, is a likely candidate for renal failure.
The primary cause of hypotension is a deficiency in blood volume. Whatabout a deficiency of the sympathetic nervous system? We could seldom demonstratesuch a deficiency. Vasoconstrictors have little or no place in the treatmentof shock in the battle casualty. Their place is limited to meeting a deficiencyin the function of the autonomic nervous system. This deficiency has beenrecognized only when the system was blocked by anesthesia or when therewas an anatomical wound of the central nervous system. We have repeatedlytreated the casualty with postoperative, refractory shock with vasoconstrictors.The blood pressure could be titrated for a few hours (fig. 4, A and B)but death was inevitable. To repeat, vasoconstrictors have an extremelylimited place in the treatment of wound shock in the battle casualty.
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Clinical experience and blood volume measurements demonstrated the valueof massive transfusions. In spite of continued transfusion and apparenthemostasis (fig. 5, A and B) some casualties died of refractory shock followinganesthesia and operation. Lt. Strawitz was able to demonstrate pulmonaryedema at autopsy in some of these patients. I am convinced that followingmassive tranfusion, an element of cardiac failure may develop. This conceptincludes an element of cardiac failure after transfusion and anesthesia.The cause of hypotension initially is blood loss. Following anesthesiaand operation we often saw a form of secondary shock. This usually respondedto additional transfusion and represented blood volume deficiency and diminishedfunction of the sympathetic nervous system as a result of anesthesia. Thosepatients who did not respond postoperatively to blood transfusion diedwith pulmonary edema and, I believe, secondary cardiac failure. I cannotfully document our case. Studies at this time often revealed a rising plasmapotassium concentration (figs. 6, 7) and an occasional patient would respond
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dramatically to an infusion of calcium (fig. 8). Strawitz and Meroneyhave suggested the possible interrelationship of these three observations.They may be pointing to a citrate toxicity in the face of continuing transfusionsand a relative hepatic insufficiency.
We speak of circulatory failure meaning the failure of circulation withinthe vascular tree. What we are really interested in is the "circulation"or diffusion between cells and extracellular fluid and between extracellularfluid and blood. This extravascular "circulation" or diffusionis the factor which determines cellular function and life.
Capillary circulation is only the means of providing it. A rough approximationof this total body "circulation" or mixing can be gained fromexperiments with deuterium oxide. Schloerb has previously demonstratedthat when the deuterium oxide was given intravenously to a normal subject,diffusion from the blood was immediate and equilibration occurred quiterapidly. In our studies of total body diffusion and mixing, the mixingwas slightly slower, but when deuterium oxide was given intravenously,the resultant curve, the deuterium concen-
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tration in venous blood of the opposite arm, reveals the rapid mixingand diffusion (fig. 9). A similar study from a patient in shock demonstratesthe greatly retarded mixing. This is hardly due to a slower circulationtime. It is due to a decrease in the effective capillary circulation-andso in the extracellular mixing and diffusion (fig. 10).
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This decrease in the effectiveness of the total body circulation leadsto an exaggeration or aberration of the response of the function of everyorgan. If shock does not persist too long, no dangerous failure in organfunction could be found. The blood volume is decreased and the total circulationis depressed. The hematocrit falls in extremity wounds and rises afterabdominal wounds. The plasma
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sodium falls and the plasma potassium may rise. The function of theautonomic nervous system appears clinically in tact as evidenced by ourclinical studies and the studies of Captain Stahl. The adrenal corticalresponse develops rapidly in spite of severe shock as indicated by thefall in eosinophile counts, the urinary retention of sodium and water,the diuresis of potassium, and the increased excretion of corticosteriods.Hepatic function, as measured by the above standard liver function tests,is depressed, but as measured by the more vital tests of metabolism appearsgenerally adequate. Renal function appears in some aspects to be markedlydepressed, presumably because of an exaggerated renal vasoconstriction.The clotting mechanism, the hematologic response and the bacterial defenseall appear adequate in face of shock of short duration.
If the shock continues for a long period of time, cellular damage becomesso severe that the cells, organs or systems may lose their function. Itmay be the heart or brain which gives out first. Dr. Shorr feels that itis the liver which by release of ferratin, a vasodilator, makes prolongedshock refractory. Our studies with Dr. Shorr indicate that many of thecasualties, who had been resuscitated from critical injuries, maintaineda positive V. D. M. test (ferritinemia) for several days. Dr. Fine believesit is the bowel which is the most sensitive and which by the release ofbacterial toxins makes pro-
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longed shock refractory. We were seldom able to obtain bacterial growthfrom blood cultures on 170 of the most severely injured casualties. Inour experience, kidney damage appeared to be the residual damage in casualtieswho barely lived.
In summary, the wound is a dynamic, not a static injury and continuesto insult the body. The insult is greatly lessened by débridement.The treatment of wound shock is, first, a restoration and maintenance ofthe blood volume, preferably with blood, and second, surgical correctionof the wound. The body responds in its entirety to severe trauma. Anesthesia,by blocking this response, is a tremendous injury to such a casualty. Althoughanesthesia is necessary in order to lessen the influence of the wound,it, per se, temporarily furthers the injury.
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At an average time of 3.5 hours after injury, irreversible shock wasnot recognized prior to anesthesia in 4,000 Korean casualties. Followinganesthesia and operation, hypotension may be quite refractory but willcharacteristically respond to continued transfusion. Even after the useof massive transfusions, the blood volume was often surprisingly low.
Following injury, the function of every system and organ in the bodyappears to be altered. The alteration is proportional, in magnitude andduration, to the magnitude of the original injury. Hypotension characteristicallyaccentuates the changes.
What are the problems for continued investigation? I should suggestthe following:
1. A continued survey of resuscitation at the battalion level.
2. Improved methods of controlling hemorrhage.
3. The effect of anesthesia on the circulation.
4. The etiology, prevention and treatment of post-traumatic renal insufficiency.
5. The fate of transfused blood in the injured man.
6. The development of a better plasma volume expander.
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7. The treatment of casualties with abdominal injuries.
8. The study of the wound, the response to injury, the resuscitative toolsand methods. This must be the approach rather than a study of the hypotensivestate, per se.
