Resuscitation of the Battle Casualty: A Résumé
Captain John M. Howard, MC, USAR
Section I. Injury and Wound Surgery
The battle wound is a dynamic injury, not a static one. It continues to injure the body for a period of days or weeks, and not simply for a period of hours. As the result of the continuing, deleterious effect of major injury, the body responds in toto. Every system, every organ, and presumably every cell in the body, respond to major trauma. This response is not a response of the moment, but a continuing response for days and weeks. The older concept, that the injury was a momentary insult and that an injured man either lived or died as a result of the initial insult, is incorrect. Under this concept, since the injury was a thing of the past, resuscitation could be directed only at its systematic effect. Such a concept is untenable today. The wound is dynamic--past, present, and future--and resuscitation must first include efforts to minimize or reverse the element of continued insult and then include efforts to correct its previous damage. First stop the injury; and then correct its previous damage. This basic concept was developed by Trueta in the Spanish Civil War and later by the surgeons of World War II.
What is the nature of the injury from which one resuscitates the casualty? There are at least four components to the battle injury, any of which may predominate or prove fatal, if left untreated. These are: (1) destruction of tissue, (2) loss of blood, (3) breaks in the defense against bacteria, and (4) occurrence of mechanical defects which may threaten life, limb, or function. A fifth, which ultimately may prove of importance, is the direct transmission of energy from the missile to the entire body, depicted only locally as tissue destruction. Functional derangements, far removed from the missile, may be caused by the direct transmission of energy just as is the case of an electric shock.
The first four components must he corrected, for any one of these may produce a progressive injury. Blood, plasma, and electrolytes are lost continuously from the wound or into the injured tissue. Products of tissue degeneration and bacterial toxins are continuously absorbed from the wound. This new element in the circulation may be working to the net disadvantage of the body. One of the major aims
in the preparation of the casualty is to minimize the effects of the wound by surgical excision. The above points are illustrated in the following outline:
The Battle Wound
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 defects. This is a continuing response of every organ and system which has been studied.
3. Anesthesia blocks part of the patient`s response and therefore, at least for the moment, furthers the injury.
The response, like the injury, is continuous. Its magnitude and duration appear to be proportional to the magnitude of injury.
The outline of the relationship of a specific response to a specific element of injury is an oversimplification; and it is used here only to demonstrate a philosophical approach to the problem. Under each specific element of injury is listed a variety of specific responses.
Tissue destruction: (1) pain and apprehension, (2) local vascular constriction and retraction, (3) inflammation, (4) shifts of water and electrolytes, (5) paralytic ileus, (6) metabolic débridement of the wound (internal débridement), (7) tissue slough (external débridement), and (8) wound healing.
Blood loss: (1) the response of the autonomic nervous system, (2) increased cardiac activity, (3) the adrenal cortical response, (4) renal vasoconstriction, (5) increased production of red blood cells, (6) increased production of plasma proteins, and (7) increased production of clotting factors.
Bacterial contamination: (1) antibody formation, and (2) leukocytic response.
Mechanical defects: (1) increased cardiac or respiratory activity to overcome effects of specific defects, and (2) muscle splinting.
Nature has effective means of controlling hemorrhage, replacing blood volume, elevating blood pressure, resisting infection, and débriding dead tissue. Yet nature`s methods may be inadequate to meet the needs of the critically injured man. It is therefore necessary to recognize the major components of injury and the major deficiencies in response, to correct the former, and to augment the latter. The over-all problem is summarized in Figure 1.
FIGURE1. Schematic diagram of dynamic effects of Injury.
The Local Wound
In one sense, the magnitude of a wound is determined by the amount of energy transmitted from the wounding agent to the body. This transmission of energy is dependent, quantitatively, upon the mass of the wounding agent, its velocity, and the resistance offered by the body.
The most massive wounds encountered in military surgery are the traumatic amputations which occur in land-mine warfare. Clinical experience has clearly indicated that a traumatic amputation of the foot at the ankle is not nearly so severe an injury as a traumatic amputation of the mid-thigh. The force required to amputate a foot at an ankle is presumably less than the force required to sever the femur and its surrounding muscles. Following transfusion, the casualty with the wound at the ankle responds rapidly in a characteristic manner, whereas the casualty with the femoral wound responds
slowly. This is a fact which maybe due partially to differences in hemeostasis.
The extent of tissue injury resulting from a bilateral traumatic amputation probably includes every cell in the body. The force applied to the lower extremities is severe enough to sever the extremities. Tissue adjacent to the line of amputation is nonviable. Tissue somewhat further away may be nonfunctional but viable. The changes may be reversible. The energy transmission does not stop at this level, however, as the man may be hurled several yards away. Every cell in the body may prove to be affected somewhat like an electrical charge. Such a concept may explain the mechanism of death in some of the men who are killed instantly.
By the same logic, an open fracture is a more severe injury than a simple, soft-tissue injury, as a greater wounding force was expended in producing it.
Working with small, high-velocity missiles, investigators at the Army Chemical Center demonstrated the large cavity of destruction which results from the indirect transmission of energy as a missile passes through tissue. This cavity persists for a fraction of a second only; but the damage to the tissue persists much longer. By this same mechanism, dirt, bacteria, fragments of cloth, and fragments of detached tissue may be scattered over a wide area. Frequently the tissue damage due to this indirect injury may be detectable clinically.
The following injuries have been noted as a result of relatively low-velocity, small-arms missiles:
1. A small wound of entrance in the right upper quadrant of the abdomen and a small wound exit in the back. The wound of the liver was the size of a double fist.
2. A small perforating wound of the arm, complicated by loss of function of the median nerve. Exploration of the wound revealed no evidence of direct injury to the nerve-an observation made rather frequently.
3. A penetrating wound of the lower thigh, with a cold pulseless foot. Exploration of the wound revealed spasm of the femoral artery without evidence that the vessel had been touched by the bullet.
4. A tangential wound of the chest wall, with the pathway of the missile lying external to a rib. Films revealed a massive hematoma of the lung.
5. Wounds of entrance and exit, each 1.0 cm. in diameter in the calf; and a wound of the gastrocnemius muscle the size of one`s fist. Such soft-tissue wounds have been seen repeatedly.
6. A perforating wound adjacent to the vertebral column, without radiological, operative, or autopsy evidence of vertebral injury; yet the patient developed a delayed paralysis of the spinal cord.
The wounds of entrance and exit, as indicated above, do not necessarily depict the degree of injury lateral to the missile`s tract; nor do they depict the magnitude of tissue destruction in the underlying tissues.
Physiologic Characteristics of the Wound
Although the production of a wound by the transmission of energy is instantaneous, the effects of the wound become dynamic.
Blood loss continues into the tissues for a variable period of time. Other investigators have demonstrated the loss of albumen into traumatized tissues. Moreover, for an unknown period of time, the loss of blood and plasma is a continuing loss.
Green and Stoner described evidence of the possible toxicity of absorbed products of muscle degeneration. Such toxins from tissue breakdown, as well as toxins from bacterial proliferation may have a systemic effect. Creatine may be excreted in large amounts after severe extremity wounds. These changes are continuing processes. The continued presence of nonviable tissue has a profound effect on the systemic response to injury, and undoubtedly it represents a continuing injury of major importance. Conversely, radical débridement may be followed by a rapid subsidence of the systemic reaction.
The continued metabolic response imposed by the wound is an additional factor which makes the wound function similarly to a vital organ.
The injury has been discussed as an injury of the entire body, with emphasis on the local tissue destruction. It should also be emphasized that certain wounds specifically affect the function of an entire system. For example, a wound of the jejunum results in a paralytic ileus of the entire gastrointestinal tract. An open wound of the chest affects the efficiency of the entire respiratory system. A wound of the brain may specifically affect the function of the entire nervous system.
These examples demonstrate the fact that severe trauma may have a local mechanical effect, a specific systemic effect, and a nonspecific effect on every cell of the body. The mechanisms involved in the causation of these effects appear to be physical (mechanical), neural, and humoral.
The Role of Wound Surgery
As long as nonviable tissue remains in a wound, the loss of blood and plasma continues; and the absorption of toxins of bacterial and tissue origin continues. Under these conditions, bacteria (including clostridia) may gain protection in the nonviable tissue outside the range of the defensive blood barrier. For these reasons, it is urgent that the nonviable tissue be excised as early as possible. The surgeon
excises the nonviable tissue and calls the procedure débridement. If he fails to débride the wound, nature does it for him. However, 2 weeks` time is required by nature; and the process is called sloughing. The rationale of débridement is: (1) to minimize the loss of blood and plasma, (2) to absorb bacteria or other toxins, and (3) to remove the dead tissue in order to effect proper circulation to the edges of the wound. In carrying out this procedure, only the nonviable tissue is excised. Some tissue may be injured but it is still viable, and it should not be excised.
The role of immediate surgery is to control hemorrhage, to determine the extent of injury, to excise nonviable tissue, to remove foreign bodies, to repair visceral, arterial, and other mechanical defects, and to prevent fluid collections by drainage.
The battle wound is a contaminated wound. Its bacterial flora usually includes clostridia, as well as a mixed aerobic flora. However, this may not be the basic reason for leaving wounds open after primary surgery. A contaminated wound can often be closed if it has been adequately débrided. In the patients studied in Korea (where the average evacuation time was 3.5 hours), personal experience included the débridement and primary closure of 20 soft-tissue wounds of muscle and an additional 20 soft-tissue wounds, including injuries to major arteries. Selection of wounds was based on the adequacy of débridement. They were small wounds, but contaminated. All 40 healed primarily. In their early management, wounds are left open for fear of inadequate débridement and resultant infection. There are several reasons why débridement may be inadequate. Sometimes adequate exposure may be almost unobtainable without creating serious deformities. After exposure, it may he quite difficult to delineate viable from nonviable tissue. Bleeding from tissue is nota reliable sign of visibility; nor is color of tissue a reliable index. The safest criterion is the contractility of muscle. Although excision of all noncontractile muscle is a safe index, it may require radical surgery, since the loss of contractility may be a reversible process. To date, although contractility is not completely satisfactory, it is perhaps the safest criterion.
As a generalization, it would appear that the better the natural blood supply to an area, the less tissue destruction there will be adjacent to a given missile trace and the more conservative the débridement required. For this reason, a functional compromise may be made and wounds of the scalp, face, thorax, stomach, small bowel, and blood vessels may be treated by a primary closure which results in normal healing in most instances.
Because of the fear of inadequate débridement and because of resultant dead space in the large wounds, primary débridement and delayed closure of soft-tissue wounds remain the soundest policy for most battle wounds. Under conditions in Korea during 1952 and
1953, where débridement was early, antibiotic therapy and tetanus prophylaxis were routine; and life-endangering infections were seldom encountered. The writer did not personally observe a case of tetanus. Gas gangrene and meningitis reached an all-time low in military medicine.
Section II. Shock and Transfusion
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, as all are entwined in the clinical syndromes found in the wounded soldier.
As more is learned about the nature of injury and the body`s response to injury, the term shock will be discarded and in its place terms used will be the specific injury and the specific response. Such a step is almost justifiable now. The value of 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 because of a primary deficiency in cardiac output. An open chest wound may produce hypotension presumably because of loss of the thoracic pump mechanism and result in a decrease in return of blood to the right heart and a diminution of cardiac output. These are specific. wounds which cause specific deficiencies and require specific therapy. Classifying all such patients together many 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. During World War II, the Board for the Study of the Severely Wounded pointed out that hypotension may have many causes; but the chief cause in most battle casualties is a deficiency in blood volume.
This discussion of shock deals primarily with patients who have injuries of the abdomen and extremities. The present concept of shock, as developed in the Korean studies, is based on a knowledge of the nature of the injury and the body`s response to the injury. The thoughts expressed here grew out of many informal conversations held at the litters of casualties at the 46th Surgical Hospital (Mobile Army) and in the laboratory of the Surgical Research Team of Korea. Many of the expressions are not. original with this writer; and much of the work mentioned is the result of combined experiences.
When a patient has sustained a severe injury, there is a response on the part of every organ in the body in an attempt to compensate for and heal the injury. Like life itself, this compensatory mechanism is an interdependent mechanism; and it is dependent upon the circulation of blood from one capillary bed to another. The response is a continuing function. One element of the injury is blood loss. When blood loss is greater than 20 percent, 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, which is produced by blood loss, therefore furthers the injury by destroying the defense mechanisms.
Shock may be defined as the clinical picture of an inadequate circulation following trauma. It is due initially to an inadequate volume of blood in circulation.
A massive wound, as stated previously, includes at least four elements of injury; and blood loss is only one of these elements. The others are tissue destruction, mechanical defects, and bacterial contamination. All of these elements of the wound produce a deleterious effect, frequently referred to as wound shock.
Tissue destruction produces a dynamic shock. It is not an injury which occurs for the moment only. Blood continues to be lost into the wound, while the toxins from bacteria and destroyed tissue are absorbed.
The entire body responds in order to meet the continuing injury. As a result of this response, compensation of the circulation may result. If the initial trauma is too great or if it is repeated and the resultant blood loss is excessive, circulatory insufficiency results. This does not imply a decompensation of the peripheral vascular mechanism. The autonomic system, heart, and peripheral vascular bed maybe functioning maximally. If the injury and blood loss are of such magnitude that the compensatory mechanism cannot maintain an adequate circulation, hypotension results.
Most of the studies of shock have centered around the loss of blood; and herein lies the crux of the problem. Studies in the Korean conflict confirmed the earlier observations that hypotension results from a rapid loss of approximately 25 percent of the blood volume. Up to this point, the heart and autonomic nervous system can compensate for the loss by increased cardiac rate and vasoconstriction in order to maintain a normal pressure. After the rapid loss of 25 percent (about 1,200 cc.), hypotension develops and, if there is a rapid loss of up to 40 percent (2,000 cc.), hypotension is profound.
Observations at the forward surgical hospital indicated that this hypotension could invariably be reversed before anesthesia, if the central nervous system was intact and if hemorrhage could be con-
trolled. There were no exceptions among nearly 5,000 casualties. Furthermore, in the resuscitation of these 5,000 battle casualties within an average time of 3.5 hours after injury, irreversible shock was not recognized prior to anesthesia provided hemorrhage had been controlled and provided no injury had occurred to the central nervous system. At this early stage, continued hypotension was the result of either continued hemorrhage or inadequate transfusion. Anesthesia, however, blocks part of the compensatory mechanism; and it may convert the compensated circulatory system to a state of profound shock. Moreover, shock may become extreme after anesthesia; and occasionally it may prove fatal if there is no response to repeated transfusions.
FIGURE 2. Hemorrhagic shock following the rapid loss of 50 percent of the blood volume.
The purpose of the circulatory system is to carry substances from one capillary bed to another, for instance, from lungs to limb, from liver to brain, from bowel to liver or to heart. Circulatory failure is a failure of capillary circulation. This failure is brought on by a reduction in the circulating blood volume. If the volume is suddenly reduced 50 percent, circulatory failure is profound and the blood pressure is unobtainable (Fig. 2). Under these conditions, total blood volume, plasma volume, and red-cell mass are each reduced by 50 percent. Death is imminent. If the 2,500 cc. loss of blood is replaced by dextran in such an amount that the total blood volume is
restored, the red-cell mass remains at the low volume of 1,125 cc. and produces a lowering in hematocrit to 22.5 percent. The red-cell mass, therefore, has not undergone any change. Upon restoration of blood volume, the patient will respond by a return of his blood pressure to normal; but his pulse rate will be somewhat fast, although slower than before therapy (Fig. 3). Proportionally, the reserve is far greater in red-cell mass than in blood volume. Circulating blood volume and capillary flow or pressure are the important elements. They are maintained by the use of plasma-volume expanders. These expanders proved to be satisfactory for use in the forward areas, where there was unavailability of whole blood.
FIGURE3. Schematic diagram of blood volume after dextran. Plasma volume is expanded by dextran and blood pressure rises. This shows the reserve in red cell mass which is greater, percentage-wise, than the reserve in blood volume.
The value of whole blood transfusions was recognized in World War II. In Korea, the helicopter permitted the treatment of many casualties who, under previous battle conditions, might have died in transit or would have been considered hopelessly injured. Blood given without cross matching was literally poured into these wounded soldiers. This experience with massive transfusions was unprecedented. Often the question was raised as to whether or not an excessive amount of blood bad been used. Clinical experience demonstrated that, if transfusion was slowed, hypotension and death resulted.
The summary of studies in blood volume following operation by Prentice and his associates unequivocally states the justification for massive transfusions in most of the severely injured. Both clinical experience and blood volume studies indicated that over transfusion rarely occurred.1 3
Artz summarized the studies of 38 consecutive patients whose blood pressure at the time of admission to the hospital was zero as measured clinically. During the first 24 hours, 12 of the patients required less than 15 pints of blood. No fatality occurred. There were 26 patients who required more than 15 pints of blood; and the case fatality rate was 54 percent. This study demonstrates that the amount of blood required for resuscitation is a better index of prognosis than is the blood pressure at the time of admission. In the group requiring more than 15 pints, the case fatality rate among the 10 patients with wounds limited to the abdomen was 90 percent in contradistinction to a case fatality rate of only 22 percent in the nine casualties with wounds of the extremities. This latter comparison indicates the difficulty in controlling intra-abdominal hemorrhage. More immediate and beneficial results will be obtained from further studies on methods of controlling hemorrhage rather than from studies on the mechanisms of late shock.
In the same summary, 84 casualties (irrespective of blood pressure on admission) required 15 or more pints of blood in the first 24 hours. Continued hemorrhage was again recognized as a major factor accounting for 16 deaths. The data of Prentice and his colleagues indicated that many of the others died of deficiency in blood volume, despite massive transfusion and apparent hemiostasis. Furthermore, a sharp difference was noted between the mortality in the patients with abdominal wounds and those with extremity wounds.
The final statement of these investigators was that, in this group requiring massive transfusion, posttraumatic renal insufficiency developed most frequently. This complication is a director indirect result of the magnitude of the wound and the severity of the shock. Posttraumatic renal insufficiency cannot be predicted by evaluating the magnitude of the wound or the severity of the hypotension at the time of admission. It can best be predicted by response to transfusion. A hypotensive, seriously wounded patient 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. A deficiency of the sympathetic nervous system could seldom be demonstrated. At present, vasoconstrictors would appear to have only a limited place in the treatment of shock in a young soldier who becomes a battle casualty. Their place is limited to meeting a deficiency in the
function of the autonomic nervous system, a deficiency which was recognized only when the system was blocked by anesthesia or when there was an anatomic wound of the central nervous system. Repeated studies were made of the role of vasoconstrictors in the treatment of the casualty with postoperative refractory shock. The blood pressure could be maintained for a few hours; but death was almost inevitable.
Clinical experience and blood-volume measurements demonstrated the value of massive transfusions. In spite of continued transfusion and apparent hemostasis, some casualties died following anesthesia and operation from refractory shock. In a few of these patients, pulmonary edema was demonstrated at autopsy. Although the cause of hypotension initially was blood loss, it appeared evident that cardiac failure might develop following massive transfusion. Secondary shock was not infrequent following anesthesia and operation. This type of shock usually responded to additional transfusion, as it represented blood-volume deficiency and possibly a continued diminution in the function of the sympathetic nervous system due to the anesthesia. The occasional patient who did not respond postoperatively to blood transfusion died with pulmonary edema and, presumably, cardiac failure. Studies of the seriously injured patients on the day after operation often revealed a transient rise in the potassium concentration of the plasma; and an occasional patient showed a dramatic response to an infusion of calcium gluconate.
Circulatory failure means the failure of circulation within the vascular tree. Of greater interest 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. Capillary circulation is the only means of providing it. A rough approximation of this total body circulation, or mixing, can be gained from experiments with deuterium oxide. When deuterium oxide is given intravenously to a normal subject, diffusion from the blood is immediate and equilibration occurs quite rapidly. In our studies of total-body diffusion and mixing, the mixing was slightly slower; but, when deuterium oxide was given intravenously, the result ant curve--the deuterium concentration in venous blood of the opposite arm--revealed the rapid mixing and diffusion. A similar study of a patient in shock demonstrated a greatly retarded mixing. This could scarcely be due to a slower circulation time. It was because of a decrease in the effective capillary circulation, i.e., in the extracellular and intracellular diffusion.
This decrease in the effectiveness of the total-body circulation leads to an exaggeration or deviation of the response of the function of every organ. If shock did not persist too bug, no dangerous failure in organ function was found. The blood volume was decreased and the total circulation was depressed. The hematocrit fell following wounds of the extremity and rose after abdominal wounds. The
plasma sodium fell and sometimes the plasma potassium rose. The function of the autonomic nervous system appeared clinically intact, as evidenced by clinical studies and by the functional studies by Stahl. The adrenal cortical response developed rapidly, in spite of severe shock, as indicated by: (1) the fall in eosinophile counts, (2) the urinary retention of sodium and water, (3) the diuresis of potassium, and (4) the increased excretion of corticosteroids. Hepatic function, as measured by standard liver function tests, was depressed; but as measured by the more vital tests of metabolism it appeared generally adequate. Renal function appeared in some aspects to be markedly depressed, presumably due to an exaggerated renal vasoconstriction. The clotting mechanism, the hematologic response, the bacterial defense, all appeared adequate in the face of shock of short duration.
If shock continues for a long period of time, cellular damage becomes so severe that the cells, organs, or systems may lose their function. The heart or brain may be the first vital organ to deteriorate. Shorr felt that the liver--by release of ferratin (a vasodilator)--makes prolonged shock refractory. Studies in Korea indicated that many of the casualties who had been resuscitated from critical injuries maintained a positive V. D. M. test (ferratinemia) for several days. Fine suggests that the release of bacteria or bacterial toxins from the bowel makes prolonged shock refractory. Bacteremia was seldom demonstrable in the battle casualty and the results of cultures of peripheral blood could not be correlated with the degree or duration of shock or the ultimate fate of the casualty. In those most seriously wounded casualties in Korea who survived, renal damage appeared to be the most deleterious residual damage.
The wound is a dynamic injury--nota static one--as it continues to insult the body. The insult is greatly lessened by débridement. The initial treatment of wound shock is to restore and maintain blood volume, preferably with blood, followed by surgical correction of the wound. The body responds in its entirety to severe trauma. By blocking this response, anesthesia is an additional injury. Although anesthesia is necessary in order to correct surgically the deleterious effects of the wound, actually it furthers the injury.
At an average time of 3.5 hours after injury, irreversible shock was not recognized prior to anesthesia in several thousand casualties of the Korean conflict. Following anesthesia and operation, hypotension was occasionally quite refractory, but usually responded to continued transfusion. Even after the use of massive transfusions, the blood volume was surprisingly low.
It appears that, following injury, the function of every organ an(l system in the body is altered. The alteration is proportional to the magnitude of the original injury in both magnitude and duration. Hypotension accentuates the changes.
Because the wound produces a continuous deleterious effect, resuscitation must be continuous until the response of the body can compensate for the effect of the injury.
Section III. Clinical Experiences with Wounds of Various Anatomic Areas
The basic defects after injury center around two points: the loss of blood and the local wound. The syndromes of injury therefore vary as the blood-volume deficit varies and as the local lesion affects various functions.
Although the systemic effects of a wound are primarily due to its loss of blood, there are other specific effects of the wound. The purpose of this report is to summarize the clinical observations in the resuscitation of almost 5,000 battle casualties at the 46th Surgical Hospital (Mobile Army) in Korea.
The syndrome following wounds of the brain is dominated by the neurologic picture. The state of consciousness is depressed to a varying extent, depending upon the exact anatomic area of the wound. Blood loss is seldom a predominant feature of the injury. The pulse rate is usually slow (50-80 per minute), being about 100 in only 10 percent of the patients studied. The blood pressure varies tremendously from patient to patient. A slight hypertension of 140/80 is not infrequent, nor is a hypotensive level of 80/40.
When the systolic blood pressure was correlated preoperatively with the blood-volume deficit (Evans blue-dye method), a qualitative relationship was found. The blood loss was not of great proportion and did not exceed 30 percent in the 11 patients so studied. The peculiarity of these patients was that hypotension might follow a loss of only 10 to 15 percent of their blood volume. Furthermore, it was observed that the blood pressure of such a casualty with a moderate hypotension often responded readily to a transfusion of only 500 cc. of blood.
Severe hemorrhagic shock was almost never seen following penetrating cranial wounds. Although blood loss is a factor, the predominant defect lies not in blood loss but in loss of neural function, often including the response of the autonomic nervous system.
The therapeutic implications are obvious. Blood loss should be replaced and further brain damage should be prevented by control of bleeding and débridemeut. At a forward echelon, infection did not appear to be a major problem.
Spinal Cord Injuries
Experience with these injuries was limited. The syndrome is one of hypotension and of paralysis below the site of injury. In the injuries of the lower cord, the sensorium may be perfectly clear. One instance occurred in which the patient was lying flat, reading a newspaper. His blood pressure in the arm was unobtainable and he was anuric. He died a few hours later, but his sensorium remained clear until shortly before death. His pulse was scarcely palpable at any time, a feature which could not be satisfactorily explained although the observation was confirmed in two subsequent patients.
The primary defect is not blood loss; and fatal pulmonary edema resulted when this fact was not recognized until overtransfusion had occurred. The primary defect is loss of function of the autonomic nervous system and possibly loss of proprioceptive reflexes to the cardiovascular system. Therapy is unsatisfactory, consisting at present of replacement of blood loss, support with vasoconstrictors, and operative débridement and decompression.
Severe chest injuries were rather infrequent at the hospital, partly because of the protection offered by the armored vest and partly because of immediate fatalities from the more serious injuries
Two defects occur in a penetrating chest wound. One is blood loss; the second is an open thorax. The low pressure in the pulmonary system seldom permits rapid bleeding from the lung, although bleeding from intercostal arteries may be quite brisk. Blood loss may reach serious proportions as bleeding continues. However, hypotension is due, in part, to the open thorax. Closure of the open wound restores the effectiveness of the thoracic pump mechanism; hence it is an integral factor in correcting the basic defects. Then thoracotomy becomes necessary in this group of patients. It should be recognized that the open thorax and the lateral position of the patient contribute to the resulting hypotension. Failure to take cognizance of this fact in three casualties and to attribute the hypotension to continued blood-volume deficit. led to overtransfusion to a serious extent.
These are wounds in which hemorrhage is the primary injury. Tissue damage may be minimal and the responsiveness of the patient appears intact. As a result, the casualty often exhibits a marked vasoconstriction and tachycardia. By these mechanisms his systolic pressure is maintained at a near-normal level until a critical blood deficit is reached, after which the pressure falls rapidly. If the hypotension is not maintained for a prolonged time, replacement of blood volume coincides with a prompt restoration of a normal blood pressure. Therapy of this patient is not a problem. Because of the normal
blood pressure, the blood-volume deficit may not be appreciated prior to anesthesia and a severe hypotension may follow induction. Because of the frequency of this error in judgment, the surgeons developed the maxim "Give the patient with an arterial injury a liter [of blood] more than he appears to need."
This is a far different wound from the simple, arterial wound. It results from the transmission of a tremendous amount of energy from an exploding mine or shell fragment. The tissue injury extends throughout the extremity if not throughout the body. There is local hemorrhage, bone, and muscle destruction. The relationship of muscle destruction and hemorrhage in producing the syndrome is not yet clear, but many of these patients respond very slowly to transfusion.
A bilateral, traumatic amputation of the thigh is the most massive injury seen in battle. The blood pressure on admission is usually imperceptible and the response to transfusion is very sluggish. This patient`s defect is not explained on the basis of external blood loss only; and sometimes it cannot be explained. This patient represents shock in its most severe form--hypotension from blood loss and tissue injury, with possible impairment of the compensatory mechanism.
Many of the major therapeutic problems lie in this group of casualties. The extent of injury varies tremendously. Perforations of the spleen and stomach offer few problems. Perforations of the liver, kidney, small intestine (especially duodenum), or colon increase the gravity of the injury. Perforation of the inferior vena cava or the iliac, renal, or other major vessels, leads to critical problems in restoration and maintenance of blood volume. Hemorrhage may be so rapid that the blood-volume deficit cannot be corrected. The induction of anesthesia to control hemorrhage in such a patient may prove fatal.
The initial syndrome in the more severe injuries is that of the typical shock picture of hypotension and tachycardia. The hypotension is sometimes resistant to transfusion. These patients, having abdominal wounds complicated by severe hemorrhage, constitute the majority of fatalities. Progress will result by finding means of controlling hemorrhage and replacing blood-volume deficit prior to the added insult of general or spinal anesthesia. One obvious clinical lesson had to be relearned; it was not to transfuse into the veins of the lower extremities when injury to the inferior vena cava was a possibility.
The peculiarities of abdominal injuries, which are shared in several aspects with the most profound of the extremity wounds, are the resistant hypotension, the high incidence of postoperative hypotension, the relatively high incidence of posttraumatic anuria, paralytic ileus, and hemoconcentration. The basic factors underlying these phenomena are not understood.
This injury is characterized by profound shock and it was seen most frequently in crushing nonpenetrating injuries. Like the occasional patient with acute pancreatitis, the hypotension seems out of proportion to the blood loss and responds slowly to transfusion.
Fracture of Long Bones
This injury, like the traumatic amputation of the foot at the ankle, is one of the few wounds associated with severe pain. The peculiarity of the vascular response is the high incidence of hypertension. At the time of admission, many of the patients have a systolic pressure above 150 and sometimes as high as 240 mm. mercury. The pulse may be rapid; more frequently, however, it. is between 60 and 80. The skin is warm; and the pulse volume is fairly good. Relief of pain may be obtained and the patient may fall asleep. Nevertheless, hypertension usually persists. It is dropped sharply by blockade of the autonomic ganglia with hexamethonium. The hypertension is undoubtedly mediated through the autonomic nervous system. Although these patients frequently demonstrated a precipitous drop in pressure following pentothal induction, their subsequent course was smooth.
In the presence of an ischemic, nonviable limb, shock may be somewhat refractory to transfusion. To date, an occasional, unexpected death within the first 24 to 48 hours after an injury can be explained only on the basic of toxicity or continued insult from such a wound.
Each organ or system serves an integral function in the body`s economy. To injure a specific system is to disrupt at least one function of the body. It is, therefore, not surprising that wounds of various anatomic areas produce different defects and present different clinical manifestations.
Recognition of the clinical manifestations of injury and an understanding of the underlying physiologic alterations are not only essential to good clinical surgery, but they are essential to further progress.
1. Prentice, T. C., Olney, J. M., Jr., Artz, C. P., and Howard, J. M.: Studies of Blood Volume and Transfusion Therapy in the Korean Battle Casualty. Surg., Gynec. & Obst. 99: 542, 1954 (Chapter 9 in Volume II of this series).
2. Stahl, R. R., Artz, C. P., Howard, M. M., and Simeone, F. A.: Studies of the Response of the Autonomic Nervous System Following Combat Injury. Surg., Gynec. & Obst. .99: 595, 1954 (Chapter 6 in Volume I of this series).
3. Artz, C. P., Howard, J. M., Sako, Y., Bronwell. A. W., and Prentice, T.: Clinical Experiences in the Early Management of the Most Severely Injured Battle Casualties. Ann. Surg. 141:285, 1955 (Chapter 2 of this volume).