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Shock

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 field of trauma: the wounding agents, the nature of the injuries, the body's response to injury, the characteristics of the resuscitative agents, the effectiveness 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 to injury, we shall, as so fittingly suggested by Green and Stoner, discard the term shock and speak of the specific injury and the specific resultant deficiency and response. We can almost justify such a step now. The value in retaining such an all-inclusive term is only to focus attention on the serious deficiency of the circulatory system. There is no common cause of hypotension following injury and therefore no common therapy. A wound of the central nervous system may produce hypotension by injury to the sympathetic nervous system. An injury to the heart or pericardium may produce hypotension due to a primary deficiency in cardiac output. An open chest wound may produce hypotension due presumably to a loss of the thoracic pump mechanism and so a decrease in return of blood to the right side of the heart with a resultant decrease in cardiac output. These are specific wounds causing specific deficiencies and requiring specific therapy. To class these patients together under any single diagnosis or plan of therapy will 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 gravity of the situation in the individual patient. Although hypotension may have many causes, the chief factor in most casualties, as was pointed out by tbe Board for the Study of the Severely Wounded, is a deficiency in blood volume. It is this group of patients with injuries primarily of the abdomen and extremities with whom we are chiefly concerned.


*Presented 21 April 1954, to the Course on Recent Advances in Medicine and Surgery, Army Medical Service 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 response to the injury. Such knowledge may be summarized as follows:

    1. The battle wound is dynamic. The battle wound results in a defect which produces a continuing deleterious effect. This continuing deleterious effect must be minimized by operative débridement.

    2. Following injury the body responds to correct the defects. This is a 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, at least for the moment, furthers the injury.

The thoughts expressed grew out of the many informal conversations held around the litters of the wounded at the 46th Surgical Hospital and around the laboratory of the Surgical Research Team in Korea. Many of the expressions are thus not original with the speaker and much of the work mentioned is the work of his colleagues.

With severe injury there is a response of every part of the body to compensate for, and reverse or heal the injury. This compensatory mechanism, like life itself, is an interdependent mechanism, dependent upon the circulation of 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 sufficient degree, an inadequate circulation results. Hypotension is one manifestation. This state of circulatory insufficiency damages the various organs taking part in the compensatory effort. Circulatory insufficiency, produced primarily by blood loss, therefore furthers the injury by destroying the defense mechanism.

Shock might therefore be defined as the clinical picture of an inadequate circulation following trauma. It is due initially to an inadequate circulating blood volume.

What is the background to wound trauma? A massive wound includes the following elements:

    1. Tissue destruction.
    2. Blood loss.
    3. Bacterial contamination.
    4. Mechanical defects.

These are the four wounding elements. A fifth which may ultimately prove of importance is the direct transmission of energy from the missile to the entire body, depicted only locally as tissue destruction. A functional aberration, quite distal to the missile, may prove to result from the direct transmission of energy just as with an elec-


252

trical shock. All of these elements of the wound produce a deleterious effect, the summation of which Churchill has termed wound shock.

Tissue destruction produces a dynamic wound. It is not an injury which occurs for the moment. As Beecher described, it continues to exert its deleterious effect. Blood is lost externally and into the injured areas. Albumin, water and electrolytes are extruded. Products of tissue breakdown are absorbed as are the toxins of bacterial action. Thus there is an exchange of substances by the circulation at the site of the undébrided wound to the net disadvantage of the body (fig.1).

FIGURE 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:


253

    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 changes following increased intracranial pressure, respiratory obstruction, cardiac tamponade, sucking chest wound, etc.

    F. Paralytic ileus.

These responses are part of the compensatory mechanisms. Most of them are a response to hemorrhage and tissue destruction.

As a result of some of these responses, compensation of the circulation may result, but if the initial trauma is too great, or is repeated, and the 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 functioning maximally. The injury and blood loss were simply so great that the compensatory mechanism could not maintain an adequate circulation. Hypotension results.

Most of the studies of shock have centered around the loss of blood and certainly this is the heart of the problem. Our studies confirmed the observation of others that with a rapid loss of 25 percent of the blood volume, hypotension develops. Up to this point, the heart and autonomic nervous system, by increased cardiac rate and vasoconstriction, can compensate for the loss to maintain a normal pressure. After the rapid loss of 25 percent (about 1,200 cc.) hypotension develops and after a rapid loss of 40 percent (2,000 cc.) hypotension is profound. Now, as seen at the forward surgical hospital, this hypotension can invariably be reversed before anesthesia if 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 an average time of 3.5 hours after injury and before anesthesia, every casualty could have


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his blood pressure restored to a normal level provided there was no injury to his central nervous system and provided hemorrhage could be controlled. To repeat, in the resuscitation of 4,000 battle casualties at an average time of 3.5 hours after injury, irreversible shock was not recognized prior to anesthesia provided hemorrhage could be controlled and there was no injury to the central nervous system. Continued hypotension, at this early time was, therefore, the result of continued hemorrhage or inadequate transfusion. Anesthesia blocks part of the compensatory mechanism and may convert the compensated circulatory system to that of a profound shock. Furthermore, after anesthesia, shock may become extremely, even fatally, resistant to transfusion therapy.

The purpose of the circulatory system is to circulate substances from one capillary bed to another-from lungs to limb, from liver to brain, from bowel to liver, to heart, etc. Circulatory failure is, therefore, a failure of capillary circulation. This failure is brought on by a reduction in the circulating blood volume and I emphasize volume. If the volume is suddenly reduced 50 percent, circulatory failure is profound with the blood pressure unobtainable (fig. 2). Under these conditions, total volume, plasma volume and red cell mass are each reduced by 50 percent. Death is imminent. Now, if the 2,500 cc. loss is replaced by dextran in such an amount that the total blood volume is restored, the red cell mass remains at the low

FIGURE 2.


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volume of 1,125 cc. so that the hematocrit drops to 22.5 percent. The red cell mass, therefore, has not been changed from that of the severe shock state. Blood volume has been restored, the patient has now responded, his blood pressure is normal, his pulse rate somewhat fast but slower than before therapy, and the man has now compensated (fig. 3). The reserve is therefore far greater in red cell mass percentagewise, than in blood volume. Circulating blood volume and capillary flow or pressure are therefore the important elements. This fact permitted the use of plasma volume expanders across the front and the response was satisfactory. This was, of course, a compromise based on the relative non-accessibility of whole blood in the 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 combined to permit the treatment of many casualties who would previously have died in transit or been considered hopeless. We literally poured blood into these men. Often the question was raised as to whether too much blood was used. We knew from experience that, if transfusion was slowed, hypotension and death resulted. Captain Prentice has summarized the blood volume studies which unequivocally demonstrated the justification for massive transfusions in most of the severely injured men. This experience with massive transfusions was unique.

FIGURE 3.


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The following three tables (tables 1, 2, and 3) demonstrate some of the practical observations. Table 1 summarizes the experience with 30 consecutive patients studied whose blood pressure at the time of admission to the hospital was zero as measured clinically. Nine patients required less than 15 pints of blood. There was no fatality. Twenty-one patients required over 15 pints and the mortality was 52 percent. In the latter group, the mortality in the seven patients with wounds limited to the abdomen was 100 percent in contradistinction to a mortality of only 12.5 percent of the eight casualties with wounds of the extremities. One of the implications of the latter comparison is the difficulty in controlling intra-abdominal hemorrhage. Greater immediate dividends will accrue from studies on methods of controlling hemorrhage than from studies on the mechanisms of late shock. Another implication from this study is that the amount of blood required for resuscitation is a better index of prognosis than is the blood pressure at the time of admission.

Table 1. Resuscitation of Battle Casualties-Admission Blood Pressure Unobtainable


Injury

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


6


50


6


3


50


3


0


0

Extremity only

14

7

8

1

12. 5

6

0

0


Total


30


37


21


11


52


9


0


0

Table 2 summarizes the experience with 60 casualties (regardless of admission blood pressure) who required 15 or more pints of blood on the day of admission. Again continued hemorrhage was recognized as a major factor accounting for 10 deaths and Captain Prentice has data to indicate that many of the others died of blood volume deficiency in spite of massive transfusion and in spite of apparent hemostasis. Again, the sharp difference is noted between the mortality in the patients with abdominal and extremity wounds.

Finally (table 3), it was in this group who required massive transfusion that post-traumatic renal insufficiency developed. This complication is a direct or indirect result of the magnitude of the wound and the severity of the shock. Post-traumatic renal insufficiency cannot be predicted by evaluating the magnitude of the wounds or the


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Table 2. Resuscitation of Battle Casualties-Patients Requiring 15 or More Pints of Blood in First 24 Hours



Injury

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


Total


60


27


45


10


34

Table 3. Resuscitation of Battle Casualties-Patients Requiring 15 or More Pints of Blood in First 24 Hours, Incidence of Renal Failure

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


Total


43


14


7


14

Incidence of clinically significant renal failure=35 percent.

severity of the hypotension at the time of admission. It can best be predicted by the response to transfusion. The hypotensive patient with serious wounds, whose blood pressure responds sluggishly to transfusion in the face of apparent hemostasis, is a likely candidate for renal failure.

The primary cause of hypotension is a deficiency in blood volume. What about a deficiency of the sympathetic nervous system? We could seldom demonstrate such a deficiency. Vasoconstrictors have little or no place in the treatment of shock in the battle casualty. Their place is limited to meeting a deficiency in the function of the autonomic nervous system. This deficiency has been recognized only when the system was blocked by anesthesia or when there was an anatomical wound of the central nervous system. We have repeatedly treated 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 extremely limited place in the treatment of wound shock in the battle casualty.


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FIGURE 4A.

Clinical experience and blood volume measurements demonstrated the value of massive transfusions. In spite of continued transfusion and apparent hemostasis (fig. 5, A and B) some casualties died of refractory shock following anesthesia and operation. Lt. Strawitz was able to demonstrate pulmonary edema at autopsy in some of these patients. I am convinced that following massive tranfusion, an element of cardiac failure may develop. This concept includes an element of cardiac failure after transfusion and anesthesia. The cause of hypotension initially is blood loss. Following anesthesia and operation we often saw a form of secondary shock. This usually responded to additional transfusion and represented blood volume deficiency and diminished function of the sympathetic nervous system as a result of anesthesia. Those patients who did not respond postoperatively to blood transfusion died with pulmonary edema and, I believe, secondary cardiac failure. I cannot fully document our case. Studies at this time often revealed a rising plasma potassium concentration (figs. 6, 7) and an occasional patient would respond


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dramatically to an infusion of calcium (fig. 8). Strawitz and Meroney have suggested the possible interrelationship of these three observations. They may be pointing to a citrate toxicity in the face of continuing transfusions and a relative hepatic insufficiency.

We speak of circulatory failure meaning the failure of circulation within the vascular tree. What we are really interested in is the "circulation" or diffusion between cells and extracellular fluid and between extracellular fluid and blood. This extravascular "circulation" or diffusion is the factor which determines cellular function and life.

FIGURE 4B.

Capillary circulation is only the means of providing it. A rough approximation of this total body "circulation" or mixing can be gained from experiments with deuterium oxide. Schloerb has previously demonstrated that when the deuterium oxide was given intravenously to a normal subject, diffusion from the blood was immediate and equilibration occurred quite rapidly. In our studies of total body diffusion and mixing, the mixing was slightly slower, but when deuterium oxide was given intravenously, the resultant curve, the deuterium concen-


260

FIGURE 5A.

FIGURE 5B.

tration in venous blood of the opposite arm, reveals the rapid mixing and diffusion (fig. 9). A similar study from a patient in shock demonstrates the greatly retarded mixing. This is hardly due to a slower circulation time. It is due to a decrease in the effective capillary circulation-and so in the extracellular mixing and diffusion (fig. 10).


261

FIGURE 6.

FIGURE 7.

This decrease in the effectiveness of the total body circulation leads to an exaggeration or aberration of the response of the function of every organ. If shock does not persist too long, no dangerous failure in organ function could be found. The blood volume is decreased and the total circulation is depressed. The hematocrit falls in extremity wounds and rises after abdominal wounds. The plasma


262

FIGURE 8.

sodium falls and the plasma potassium may rise. The function of the autonomic nervous system appears clinically in tact as evidenced by our clinical studies and the studies of Captain Stahl. The adrenal cortical response develops rapidly in spite of severe shock as indicated by the fall 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 appears generally adequate. Renal function appears in some aspects to be markedly depressed, presumably because of an exaggerated renal vasoconstriction. The clotting mechanism, the hematologic response and the bacterial defense all appear adequate in face of shock of short duration.

If the shock continues for a long period of time, cellular damage becomes so severe that the cells, organs or systems may lose their function. It may be the heart or brain which gives out first. Dr. Shorr feels that it is the liver which by release of ferratin, a vasodilator, makes prolonged shock refractory. Our studies with Dr. Shorr indicate that many of the casualties, who had been resuscitated from critical injuries, maintained a positive V. D. M. test (ferritinemia) for several days. Dr. Fine believes it is the bowel which is the most sensitive and which by the release of bacterial toxins makes pro-


263

FIGURE 9.

longed shock refractory. We were seldom able to obtain bacterial growth from blood cultures on 170 of the most severely injured casualties. In our experience, kidney damage appeared to be the residual damage in casualties who barely lived.

In summary, the wound is a dynamic, not a static injury and continues to insult the body. The insult is greatly lessened by débridement. The treatment of wound shock is, first, a restoration and maintenance of the blood volume, preferably with blood, and second, surgical correction of the wound. The body responds in its entirety to severe trauma. Anesthesia, by blocking this response, is a tremendous injury to such a casualty. Although anesthesia is necessary in order to lessen the influence of the wound, it, per se, temporarily furthers the injury.


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FIGURE 10.

At an average time of 3.5 hours after injury, irreversible shock was not recognized prior to anesthesia in 4,000 Korean casualties. Following anesthesia and operation, hypotension may be quite refractory but will characteristically respond to continued transfusion. Even after the use of massive transfusions, the blood volume was often surprisingly low.

Following injury, the function of every system and organ in the body appears to be altered. The alteration is proportional, in magnitude and duration, to the magnitude of the original injury. Hypotension characteristically accentuates the changes.

What are the problems for continued investigation? I should suggest the 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 tools and methods. This must be the approach rather than a study of the hypotensive state, per se.