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Intensive Care of the Trauma Patient
Symposium on Intensive Care Units
Intensive Care of the Trauma Patient Donald S. Gann, MD.,* and George D. Zuidema, MD.**
The intensive care of the patient who has undergone serious trauma must be directed to answer needs which arise from three factors, partially independent and partially interdependent. The first of these relates to the nature of the injury itself, which produces local, anatomical, and functional derangement and which also initiates a more widespread response. The second factor is the overall body response to trauma itself, which, although initiated by the specific injury, ranges far to involve nearly every organ system in the body. The third factor is the set of complications which arise from trauma and which are, at least in part, peculiar to the situation in the injured patient, and which result in part from the local injury and in part from the general body response.
THE NATURE OF THE INJURY In every case of severe trauma, there has been damage to some specific area or organ system. Several factors commonly accompany this injury, including hemorrhage, accumulation of tissue fluid in the injured area (so-called "third space"), and pain. The initial treatment of the trauma patient must include such factors as maintenance of an airway or its restoration, control of hemorrhage and restoration of normal functioning blood volume (by administration of blood, dextran, or electrolyte solutions), and direct attention to the injured area. This attention must be directed to precise definition of a diagnosis and to institution of therapy. Certain common complications which accompany trauma in specific areas are evident but are sufficiently common to warrant mention. These include fractures of the long bones which accompany trauma to the extremity; rupture of hollow viscera, spleen, or liver accompanying abdominal trauma; rib fracture with flail chest or pericardial infusion, *Professor of Biomedical Engineering, The Johns Hopkins University School of Medicine, Baltimore, Maryland **Professor and Chairman, Department of Surgery, The Johns Hopkins University School of Medicine, Baltimore, Maryland
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or contused lung, accompanying blows to the chest (the latter may also be a direct complication of blunt injury to the abdomen, because the sudden increase in abdominal pressure forces the diaphragm to rise rapidly against the base of the lungs); skull fracture and intracranial hemorrhage accompanying head injuries; fracture of the facial bones, and distortion of the airway accompanying injuries to the head and neck. This list is far from complete, and for extensive discussion of local injuries to specific areas and their therapy the reader is directed elsewhere. 2 • 7 While the initial treatment of the injured patient normally leads to prompt diagnosis and, where feasible, correction of the sorts of injuries outlined above, and thus generally precedes the period of intensive care, this is not always the case. The physician treating the injured patient must formulate a hierarchy of priorities for treatment; maintenance of an airway, restoration of depleted blood volume, control of bleeding, and decompression of a fractured skull or intracranial hemorrhage must take precedence over the therapy of long bone fractures and similar injuries, which can be controlled temporarily by maneuvers such as immobilization and which do not threaten the life of the patient. Accordingly, some local factors, especially pain arising from the injury, are commonly significant during the phase of intensive care. However, in severe injury this phase is normally preceded by direct surgical attack upon the injured area for the purpose of control of hemorrhage, restoration of the continuity of the intestinal tract, removal of certain contused tissues or ruptured organs, and cleansing and drainage of the contaminated peritoneal cavity.
THE BODY'S RESPONSE TO TRAUMA Tissue injury itself and the attendant hemorrhage and pain set in motion a multidimensional and widespread body response to injury which involves in rapid succession nearly every organ system within the body. Although widespread response has been organized below for ease of consideration, it should be noted that this organization is arbitrary and that the factors which have been separated below are really interconnected in a highly complex pattern. The Neurohumoral Response Tissue injury, hemorrhage, and pain promptly set in motion a set of mechanisms which have long been recognized to involve the sympathetic nervous system and to resemble an increase in its activity. However, it has become clear with increasing time that this response involves as well the increased or decreased secretion of a variety of hormones, and the list of endocrine factors which are involved in this response is extending as additional areas are studied. It does not seem unreasonable to believe that virtually every autonomic and endocrine pathway may be involved in the response. Of particular interest, in addition to the increase in sympathetic activity, are the increased secretions of cate-
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cholamines, adrenocorticotropic hormone, renin (and thus angiotensin 11), growth hormone, vasopressin, cortisol, and aldosterone. Secretion of other hormones such as insulin, follicle-stimulating hormone, and luteinizing hormone, which often antagonize the actions of the substances named above, appears to be inhibited. In addition, release into the circulation of substances which are more appropriately viewed as local hormones, such as bradykinin and the prostaglandins, appears to be increased. The actions of these substances are in general opposed to the actions of the principal hormones such as catecholamines, adrenocorticotropic hormone, and the adrenal steroids, so that they may represent a partial negative feedback response to those substances designed to control their effects more tightly. However, in the presence of massive release there is spillover of these normally local factors into the general circulation. The overall effect of this neurohumoral response appears to be to set in motion changes in circulatory, respiratory, renal, and metabolic functions, which in turn are organized to offset the effect of injury and to restore homeostasis.
Circulatory Response Even in the absence of the neurohumoral response, the vascular system contracts around a reduced blood volume. This decreases its compliance and increases its resistance. The neurohumoral response adds to this natural response and produces increased speed, increased effectiveness, and more prolonged duration. The principal effective factors are direct sympathetic innervation, and the catecholamines, angiotensin 11, and vasopressin. Circulatory compliance decreases, arterial resistance increases, and stroke work and heart rate both increase. Although these effects are opposed in part by the actions of bradykinin and the prostaglandins, the overall effect of this portion of the circulatory response is to restore venous return and cardiac output toward normal levels. In addition, as arteriolar tone increases, capillary pressure decreases. This change permits the net flow of fluid from the extracellular to the intravascular space and represents in turn the initial phase of restitution of blood volume. If this fluid remains in the circulation, the effect is accompanied by a fall in hematocrit and a decrease in blood viscosity. The fall in hematocrit is generally assumed to be on the basis of progressive hemorrhage, but actually signifies the attempt to correct it. Thus, the overall effect of this phase of the circulatory response is the beginning of restoration of blood volume toward normal. Within the blood itself, and at least in part as a result of action of catecholamines, aggregates of platelets tend to form. This phenomenon may give rise to a tendency towards increased clotting within the circulation. Although initially beneficial, this may lead later to further complications.
Pulmonary Response Injury, hemorrhage, and pain lead initially to an increase in ventilatory rate, in part through direct stimulation to pain pathways and in
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part through activation of chemoreceptor mechanisms. There is a fall in pC02 which is secondary to this increase in ventilatory rate, but which is also secondary to a decrease in venous return and thus to a decreased delivery to the lung of carbon dioxide formed in tissues. Whereas a fall in arterial concentration of carbon dioxide normally tends to slow the respiratory rate, this does not occur in severe injury, in part because of the delivery of an increased metabolic acid load from the periphery, and in part because of hypoxia which may accompany thoracic trauma or airway obstruction. The acid load tends to shift potassium ion from its normal place within the cells to an extracellular position as hydrogen ion moves into cells. This increase of extracellular to intracellular ratio of potassium diminishes the effectiveness of muscular contraction and thus impairs the effectiveness of the ventilatory effort. This is reflected in turn by an increased oxygen cost of breathing. As Moore has pointed out, this effect may lead in turn to further hypoxia and thus to increased acidosis, to form a vicious spiral of positive feedback should availability of oxygen or its diffusion be limited by factors such as decreased respiratory effect, pneumonitis, atelectasis, bronchospasm, or increased physiologic shunt. Despite the lifethreatening nature of some of these factors, the physiologic response of the respiratory system itself appears to be directed toward an attempt to maintain delivery of oxygen to tissue, and removal of carbon dioxide from the blood.
Metabolic Response CARBOHYDRATE METABOLISM. The breakdown of glycogen stores begins rapidly after hemorrhage, as a result of the action of epinephrine and glucagon. In addition, the conversion of amino acids into glucose (gluconeogenesis) is accelerated by the action of cortisol, which also impairs the entrance of glucose into the cells. However, glycogenolysis and gluconeogenesis increase the quantities of glucose available for glycolysis. In tissues with attendant vasoconstriction and diminished oxygen delivery the glucose cannot be completely metabolized by the tricarboxylic acid cycle, so that there is a shift from aerobic to a~aerobic metabolism. This is reflected in part by an increase of production of lactate relative to pyruvate (excess lactate) and thus to increased delivery of an acid load from the tissues. Furthermore, because of the difficulty of glucose entrance into cells and because of the overload of the glycolytic pathway, there is a transient "diabetic" response which is insulinresistant. Increased blood sugar after hemorrhage was first noted more than 100 years ago by Claude Bernard. Although it appears to have little significance of itself, it should be noted, however, that it indicates an inability of the tissues to remove glucose in a normal way. If glucose is administered in large amounts, blood concentration of this substance may be elevated and may overload renal reabsorptive mechanisms. PROTEIN METABOLISM. In most tissues, primarily as an effect of cortisol, decreased insulin, and decreased sex hormone secretion, the incorporation of amino acids into tissues is decreased. Since these tissues are normally in dynamic equilibrium, and since the movement of amino
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acids out of the cells is not impaired, there is a net catabolic effect. As nitrogen moves out of cells, potassium accompanies it, thus increasing the concentration of extracellular potassium relative to intracellular potassium. As noted above, this may impair muscular activity in striated muscle, smooth muscle, and cardiac muscle. The increased load of amino acids in turn is used primarily in gluconeogenesis as described above, and secondarily may be involved in the synthesis of new albumin. Increased quantities of albumin within the circulation act in turn by increasing onc otic pressure to hold within the vascular space fluid which has moved intravascularly across the capillaries from the extravascular extracellular fluid volume. FAT METABOLISM. The catecholamines, growth hormone, adrenocorticotropic hormone, and decreased insulin secretion all combine to increase the rate of lipolysis and the movement of fatty acids to the liver from peripheral tissues. The liver in turn synthesizes and releases lipoproteins. Whereas these elements are soluble in the blood in small quantities, when they are released in large amounts they may aggregate and form fat emboli, which may in turn impair pulmonary function. However, the overall effect of the metabolic response to injury is to increase the delivery of metabolic components for incorporation into the metabolic pathways which lead to formation of adenosine triphosphate, and for wound repair. Renal Response The primary response of the kidney to hemorrhage and trauma is the diminished excretion of salt and water. In severe injury, this may be produced by fall in the rate of glomerular filtration, but this is offset, initially at least, by an increase in tone within the efferent arterioles and possibly in addition by the action of cortisol. In the absence of renal failure, the diminished excretion of sodium and water is primarily the result of increased reabsorption of these substances from the proximal tubule, which is currently viewed as a decrease in "third factor." This "factor" appears to be a set of mechanisms which may involve a hormone which has thus far defied identification, but which appears to be primarily the result of increased peritubular oncotic pressure resulting from efferent arterial constriction and maintained glomerular filtration. In addition, the adrenal hormone aldosterone promotes the absorption of sodium and water from distal sites in the nephron and also facilitates the excretion of potassium and hydrogen ions. Furthermore, increased quantities of vasopressin within the circulation promote further reabsorption of water. The overall effect of the renal response to trauma is to prevent further depletion of blood volume, and thus secondarily to aid the restitution of that volume.
THERAPEUTIC IMPLICATIONS The overall body response to trauma outlined above has specific implications in the intensive care of the traumatized patient. In general we believe that the physician can act most effectively if he recognizes
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and attempts to support, in his therapeutic maneuvers, the attempt of the body to maintain effective circulation and oxygen delivery. However, he must be aware of limitations of functional reserve and of the existing mechanisms of response which have been engaged physiologically, in order to avoid overload of the system. For example, as a result of the renal response outlined above there is an inability to excrete large amounts of salt or water. Thus, even in the presence of relative depletion of body fluids, electrolyte solutions must be administered judiciously, with reference to actual losses (or displacements into "third space") in order to prevent circulatory overload and pulmonary edema. It should be noted, as Bartter has done, that the renal response to trauma resembles that to congestive heart failure, so that in patients with the combination of trauma and congestive failure, fluid therapy requires extreme care. The measurement of central venous pressure as an index of circulating volume has attracted enthusiastic support in recent years. However, this measurement may be misleading, according to the degree of vasoconstriction and of effectiveness of the myocardium. Similarly, although they may be extremely helpful adjuvants, fluid therapy must not be based solely upon volume and osmolality of the urine, but should be determined primarily by estimates of losses or translocations of fluid and by measurement of body weight. Since acidosis is a major result of hypoperfusion and vasoconstriction, and since a decrease in pH leads to decreased efficiency of contraction of muscle, efforts must proceed to correct this condition. In particular, the apparent alkalosis early in the post-traumatic period should not lull the physician into complacency, since it results from the combination of hyperventilation and diminished delivery of carbon dioxide from the tissues. If ventilatory effectiveness diminishes, and as restitution of blood volume leads to restored delivery of carbon dioxide and lactate from tissues, the alkalosis may shift rapidly to a profound metabolic acidosis. Intravenous administration of bicarbonate ion and maintenance of blood volume and thus of perfusion appear to be the best therapeutic measures at present. Since glucose cannot be metabolized normally after trauma, its infusion in large amounts may lead to additional loss of salt and water in the urine. Far from reflecting adequate fluid replacement, this response is merely an osmotic diuresis (it does reflect continued glomerular filtration) and will lead to increased deficits of fluid. Excess glucose administration is, therefore, to be avoided. Since glucose movement into cells is impaired and since this impairment is resistant to insulin, the use of glucose and insulin to treat the hyperkalemia of acidosis and injury is not as effective as in the case of renal failure. Again, the treatment of choice seems to be infusion of bicarbonate, which moves potassium into cells in exchange for hydrogen, unless the condition is severe enough to demand hemodialysis. Acute renal failure occasionally occurs as a result, perhaps, of increased filtration of free hemoglobin or myoglobin in the face of increased salt and water reabsorption. If high concentrations of pigment
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are detected early, there appears to be some protective effect of sustained osmotic diuresis. If this approach is selected, fluid depletion can be prevented by administration of mannitol in one-half isotonic saline. 4 Should full-blown renal failure occur, therapy should be directed to fluid restriction, with administration designed only to replace losses and to minimize catabolism. In calculating fluids to be administered, the water of oxidation of foodstuffs (endogenous as well as exogenous) must be considered. Measurement of body weight is of paramount importance. The availability of safe and early hemodialysis when renal failure occurs, and prevention of renal failure by early detection, volume replacement, and osmotic diuresis, has led to removal of renal failure as a common cause of death from trauma. In attempting to support the circulation, the physician must remember that prolonged vasoconstriction will increase acidosis and thus ultimately impair cardiac function itself. Accordingly, the primary support of peripheral circulation requires restitution of blood volume rather than vasoconstrictive drugs. However, it has been suggested that inotropic agents may be effective support, particularly in elderly patients, once circulating volume has been restored. Cardiac arrest is a common problem in the trauma patient. It is commonly preceded by hypoxia and acidosis, and may be prevented by proper attention to airway, oxygenation, and metabolism. The early use of lidocaine is indicated if evidence of myocardial irritability appears. If arrest or ventricular fibrillation occurs, it should be handled in the usual way by closed chest massage and defibrillation. Intracardiac administration of lidocaine, bicarbonate, isoproterenol, or occasionally calcium may prove a useful adjuvant to treatment. Support of oxygenation is of great importance, even in non-thoracic trauma. Assisted ventilation can improve distribution of gas within the lungs and diminish the frequency of atelectasis. Ventilatory support decreases the oxygen cost of breathing and thus can break the acidotic spiral. Increased end-expiratory pressure, as in continuous positive pressure breathing, can reduce the formation of pulmonary edema. The use of high concentrations of oxygen in inspired air may be required for brief periods, but prolonged administration of oxygen is to be avoided. If ventilation is supported and if atelectasis and pneumonitis are prevented, one can avoid the need for oxygen in many cases, but not in all (see below). A final complication which may arise as a direct result of the body response to trauma is the occurrence of stress ulceration of the stomach. Such lesions may result from a shunting of blood away from the gastric mucosa by prolonged nerve stimulation or from prolonged action of cortisol, with decreased resistance of the mucosa to acid. Some physicians suggest the use of prophylactic antacid therapy. If stress ulceration occurs, it commonly presents as bleeding, and is detected by hematemesis, melena, or deterioration of vital signs. Early diagnosis and treatment, conservative if possible, are imperative; if bleeding persists, gastric resection may be necessary.
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COMPLICATIONS OF TRAUMA The morbidity of trauma can be ascribed in part to the specific injury sustained and in part to three major kinds of complications. A major cause of death following trauma which appears to be increasing in importance is post-traumatic pulmonary insufficiency. This is a condition in which the lungs appear to be congested and there is interstitital edema, and in which the major physiologic evidence is de saturation of the arterial blood, even in the presence of high inspired tension of oxygen. It is generally associated with an increased rate of ventilation, and has been called "high-output respiratory failure."3 This phenomenon is poorly understood at present. It is measured as an increase in true shunt, or decrease in the ratio of ventilation to perfusion. However, many factors which may be the result of direct injury or the result of body response to trauma may play a role in the evolution of this complication. Some of these factors may be treated specifically and others may be prevented by early recognition. They include atelectasis, pulmonary edema, decreased ventilation, pneumonitis, bronchospasm, and decreased surfactant (a secondary complication of oxygen therapy). Therapeutic maneuvers which appear to be of some effectiveness are controlled respiration with continuous positive pressure breathing to elevate end-respiratory pressure and diminish edema production, antibiotics, maintenance of a patent airway, limited use of high oxygen tensions, and in certain instances, the use of bronchodilators. It appears increasingly, however, that this complication may result not only from tissue trauma and infection but may also result from the action of certain substances released into the bloodstream, which may include bradykinin, some of the prostaglandins (particularly prostaglandin F 2a ) and serotonin and histamine released from the breakup of platelet aggregates. However, these phenomena have not been well documented and their role is difficult to evaluate, so that therapy is at best empirical. In particular, as noted above, the use of high oxygen concentration in inspired air is unsatisfactory treatment, in part because it rarely increases to normal the degree of oxygen saturation in arterial blood and in part because it acts to destroy pulmonary surfactant. The possible role of new therapeutic maneuvers, such as oxygenation of the venous blood by partial bypass through a membrane oxygenator, is incompletely evaluated at this time. In general, the therapeutic approach to this complication depends upon early recognition and a direct approach to individual aggravating or preCipitating factors as they arise and are recognized. One may hope that therapy will improve as the process becomes better understood and as methods for early diagnosis are improved. The second major general complication of trauma during the period of intensive care is delayed hemorrhage. Hemorrhage may follow the lysis of a clot or the release of vasospasm. It is relatively common from the spleen, but may occur from other organs as well. Rarely it is the result of necrosis in a wound or a complication of initial surgical maneuver.
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Stress ulcer may also be the source of bleeding. The satisfactory treatment of hemorrhage depends upon its early recognition, direct maneuvers to control it, and adequate restitution of the blood volume, using fresh blood when necessary. A third major complication of trauma in general is infection. If tracheostomy or tracheal intubation has been done in order to maintain an airway or to support ventilation, a virulent form of tracheal bronchitis is relatively common, as is bronchopneumonia. If the bowel has been ruptured, or perforated, intraperitoneal gram-negative infection, peritonitis, and at times endotoxin shock may occur. The appropriate therapy of these infections as well as infections in wounds is evident and depends upon early recognition, the use of aseptic techniques to minimize contamination, particularly in the case of tracheostomy, the judicious use of antibiotics to meet specific bacterial complications, and in the case of endotoxin shock, early diagnosis and the supplementation of antibiotic therapy with massive doses of corticosteroids. The principle of surgical drainage of abscesses is essential, when such collections can be identified.
PATIENT MONITORING The preceding comments may be taken to imply that satisfactory intensive care of the trauma patient depends in part upon basing therapeutic decisions upon an integrated overall view of the behavior, physiologic compensation, and pathologic decompensation of the many organ systems within the body. In addition, therapeutic effectiveness will be increased only as it becomes possible to diagnose complications early, or even to predict the evolution of complications such as pulmonary insufficiency. One may hope that a better integrated view and earlier diagnosis may result from improved techniques of patient monitoring applied to these patients. The monitoring system for the traumatized patient must include the measurement of multiple respiratory functions and renal function as well as measures of circulatory effectiveness. In particular, the selection of the electrocardiogram as a primary monitored variable has little to recommend it, since cardiac derangement in cases of trauma is an exceedingly late sign of disturbance, and since this disturbance may reflect circulatory inadequacy, hypoxia, acidosis or hyperkalemia. Similarly, major reliance upon arterial pressure may provide the therapeutic team with only a late index of disturbance because of the many compensatory mechanisms which are activated by trauma and hemorrhage and which act, at least in major part, to maintain arterial pressure. At this time, there has been established no generally satisfactory monitoring system for the traumatized patient, though efforts are proceeding in this direction in a number of centers. The development of these systems depends, in turn, upon the development of monitoring systems which meet three criteria.
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First, attention must be directed to the measurement of appropriate variables, which include not only those which are most easily measured but those which are most commonly deranged, and among these, those in which derangements occur earliest. These include cardiovascular variables which are measured less commonly than is arterial pressure but which may reflect early changes which either trigger or signify compensatory action to maintain mean arterial pressure. These include arterial pulse pressure, maximum dP/dt, systolic ejection time, and cardiac output. Increased emphasis must be placed on respiratory variables, including blood gases, ventilatory flow, estimates of alveolar gas concentrations and, at times, esophageal (intrathoracic) pressure. With respect to renal function, one must observe not only the rate of urine flow but also sodium concentration, osmolality, and of course body weight. Since these variables differ in their dynamic properties, they need not all be measured with equal frequency. Rather, those variables which change fastest, such as some of the cardiovascular variables, must be measured as often as beat by beat, while certain respiratory variables change little over several hours, and so may be measured less often. Second, there are sets of variables which are not themselves measurable, but which may be computed from other measurable variables. An example of these is the computation of stroke volume from high quality pressure pulse tracings. Other computations include that of oxygen consumption as the integral of the product of oxygen concentration and air flow, which appears to be a sensitive index of incipient respiratory failure, as is the computation of oxygen cost of breathing which can be derived from oxygen consumption measured at different levels of airway resistance. Furthermore, lung compliance and resistance can be computed from a frequency analysis of pressure and flow,5 so that these variables can be made accessible without an inordinate degree of invasion of the patient. The availability of these computed variables at the bedside will permit evaluation of their utility in practice. However, preliminary observations suggest that the computed variables will be useful in providing physicians with earlier warning of derangements. Finally, work is just beginning to develop monitoring systems which evaluate the response of patients to small perturbations. This approach has been exceedingly useful in the evaluation of states of physical systems and holds high promise in the area of patient monitoring. In particular, such dynamic measurements can provide not only an index of performance but also an index of the reserve which remains in various organ systems. Perhaps the evolution of an ideal program for the intensive care of the trauma patient depends predominantly on further advances in this area.
REFERENCES 1. Bartter, F. C.: Cardiac failure and hormonal control of fluid and electrolyte balance. Surg. Gynec. Obstet., 118:767,1964. 2. Ballinger, W. F., 11, Rutherford, R. B., and Zuidema, G. D., eds.: The Management of Trauma. Philadelphia, W. B. Saunders, 1968.
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3. Burke, J. F., Pontoppidan, H., and Welch, C. E.: High output respiratory failure. Ann. Surg., 158:581,1963. 4. Gann, D. S., Wright, H. K., and Newsome, H. H.: Prevention of sodium depletion during osmotic diuresis. Surg. Gynec. Obstet., 119:265,1964. 5. Hilberman, M., Schill, J. P., and Peters, R. M.: On-line digital analysis of respiratory mechanics and the automation of respirator control. J. Thorac. Cardiovasc. Surg., 58:821,1969. 6. Moore, F. D., et al.: Post-Traumatic Pulmonary Insufficiency. Philadelphia, W. B. Saunders, 1969. 7. Shires, G. T., ed.: Care ofthe Trauma Patient. New York, McGraw-Hill, 1966. The Johns Hopkins University School of Medicine Baltimore, Maryland 21205
Intensive Care of the Trauma Patient Donald S. Gann, MD.,* and George D. Zuidema, MD.**
The intensive care of the patient who has undergone serious trauma must be directed to answer needs which arise from three factors, partially independent and partially interdependent. The first of these relates to the nature of the injury itself, which produces local, anatomical, and functional derangement and which also initiates a more widespread response. The second factor is the overall body response to trauma itself, which, although initiated by the specific injury, ranges far to involve nearly every organ system in the body. The third factor is the set of complications which arise from trauma and which are, at least in part, peculiar to the situation in the injured patient, and which result in part from the local injury and in part from the general body response.
THE NATURE OF THE INJURY In every case of severe trauma, there has been damage to some specific area or organ system. Several factors commonly accompany this injury, including hemorrhage, accumulation of tissue fluid in the injured area (so-called "third space"), and pain. The initial treatment of the trauma patient must include such factors as maintenance of an airway or its restoration, control of hemorrhage and restoration of normal functioning blood volume (by administration of blood, dextran, or electrolyte solutions), and direct attention to the injured area. This attention must be directed to precise definition of a diagnosis and to institution of therapy. Certain common complications which accompany trauma in specific areas are evident but are sufficiently common to warrant mention. These include fractures of the long bones which accompany trauma to the extremity; rupture of hollow viscera, spleen, or liver accompanying abdominal trauma; rib fracture with flail chest or pericardial infusion, *Professor of Biomedical Engineering, The Johns Hopkins University School of Medicine, Baltimore, Maryland **Professor and Chairman, Department of Surgery, The Johns Hopkins University School of Medicine, Baltimore, Maryland
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or contused lung, accompanying blows to the chest (the latter may also be a direct complication of blunt injury to the abdomen, because the sudden increase in abdominal pressure forces the diaphragm to rise rapidly against the base of the lungs); skull fracture and intracranial hemorrhage accompanying head injuries; fracture of the facial bones, and distortion of the airway accompanying injuries to the head and neck. This list is far from complete, and for extensive discussion of local injuries to specific areas and their therapy the reader is directed elsewhere. 2 • 7 While the initial treatment of the injured patient normally leads to prompt diagnosis and, where feasible, correction of the sorts of injuries outlined above, and thus generally precedes the period of intensive care, this is not always the case. The physician treating the injured patient must formulate a hierarchy of priorities for treatment; maintenance of an airway, restoration of depleted blood volume, control of bleeding, and decompression of a fractured skull or intracranial hemorrhage must take precedence over the therapy of long bone fractures and similar injuries, which can be controlled temporarily by maneuvers such as immobilization and which do not threaten the life of the patient. Accordingly, some local factors, especially pain arising from the injury, are commonly significant during the phase of intensive care. However, in severe injury this phase is normally preceded by direct surgical attack upon the injured area for the purpose of control of hemorrhage, restoration of the continuity of the intestinal tract, removal of certain contused tissues or ruptured organs, and cleansing and drainage of the contaminated peritoneal cavity.
THE BODY'S RESPONSE TO TRAUMA Tissue injury itself and the attendant hemorrhage and pain set in motion a multidimensional and widespread body response to injury which involves in rapid succession nearly every organ system within the body. Although widespread response has been organized below for ease of consideration, it should be noted that this organization is arbitrary and that the factors which have been separated below are really interconnected in a highly complex pattern. The Neurohumoral Response Tissue injury, hemorrhage, and pain promptly set in motion a set of mechanisms which have long been recognized to involve the sympathetic nervous system and to resemble an increase in its activity. However, it has become clear with increasing time that this response involves as well the increased or decreased secretion of a variety of hormones, and the list of endocrine factors which are involved in this response is extending as additional areas are studied. It does not seem unreasonable to believe that virtually every autonomic and endocrine pathway may be involved in the response. Of particular interest, in addition to the increase in sympathetic activity, are the increased secretions of cate-
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cholamines, adrenocorticotropic hormone, renin (and thus angiotensin 11), growth hormone, vasopressin, cortisol, and aldosterone. Secretion of other hormones such as insulin, follicle-stimulating hormone, and luteinizing hormone, which often antagonize the actions of the substances named above, appears to be inhibited. In addition, release into the circulation of substances which are more appropriately viewed as local hormones, such as bradykinin and the prostaglandins, appears to be increased. The actions of these substances are in general opposed to the actions of the principal hormones such as catecholamines, adrenocorticotropic hormone, and the adrenal steroids, so that they may represent a partial negative feedback response to those substances designed to control their effects more tightly. However, in the presence of massive release there is spillover of these normally local factors into the general circulation. The overall effect of this neurohumoral response appears to be to set in motion changes in circulatory, respiratory, renal, and metabolic functions, which in turn are organized to offset the effect of injury and to restore homeostasis.
Circulatory Response Even in the absence of the neurohumoral response, the vascular system contracts around a reduced blood volume. This decreases its compliance and increases its resistance. The neurohumoral response adds to this natural response and produces increased speed, increased effectiveness, and more prolonged duration. The principal effective factors are direct sympathetic innervation, and the catecholamines, angiotensin 11, and vasopressin. Circulatory compliance decreases, arterial resistance increases, and stroke work and heart rate both increase. Although these effects are opposed in part by the actions of bradykinin and the prostaglandins, the overall effect of this portion of the circulatory response is to restore venous return and cardiac output toward normal levels. In addition, as arteriolar tone increases, capillary pressure decreases. This change permits the net flow of fluid from the extracellular to the intravascular space and represents in turn the initial phase of restitution of blood volume. If this fluid remains in the circulation, the effect is accompanied by a fall in hematocrit and a decrease in blood viscosity. The fall in hematocrit is generally assumed to be on the basis of progressive hemorrhage, but actually signifies the attempt to correct it. Thus, the overall effect of this phase of the circulatory response is the beginning of restoration of blood volume toward normal. Within the blood itself, and at least in part as a result of action of catecholamines, aggregates of platelets tend to form. This phenomenon may give rise to a tendency towards increased clotting within the circulation. Although initially beneficial, this may lead later to further complications.
Pulmonary Response Injury, hemorrhage, and pain lead initially to an increase in ventilatory rate, in part through direct stimulation to pain pathways and in
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part through activation of chemoreceptor mechanisms. There is a fall in pC02 which is secondary to this increase in ventilatory rate, but which is also secondary to a decrease in venous return and thus to a decreased delivery to the lung of carbon dioxide formed in tissues. Whereas a fall in arterial concentration of carbon dioxide normally tends to slow the respiratory rate, this does not occur in severe injury, in part because of the delivery of an increased metabolic acid load from the periphery, and in part because of hypoxia which may accompany thoracic trauma or airway obstruction. The acid load tends to shift potassium ion from its normal place within the cells to an extracellular position as hydrogen ion moves into cells. This increase of extracellular to intracellular ratio of potassium diminishes the effectiveness of muscular contraction and thus impairs the effectiveness of the ventilatory effort. This is reflected in turn by an increased oxygen cost of breathing. As Moore has pointed out, this effect may lead in turn to further hypoxia and thus to increased acidosis, to form a vicious spiral of positive feedback should availability of oxygen or its diffusion be limited by factors such as decreased respiratory effect, pneumonitis, atelectasis, bronchospasm, or increased physiologic shunt. Despite the lifethreatening nature of some of these factors, the physiologic response of the respiratory system itself appears to be directed toward an attempt to maintain delivery of oxygen to tissue, and removal of carbon dioxide from the blood.
Metabolic Response CARBOHYDRATE METABOLISM. The breakdown of glycogen stores begins rapidly after hemorrhage, as a result of the action of epinephrine and glucagon. In addition, the conversion of amino acids into glucose (gluconeogenesis) is accelerated by the action of cortisol, which also impairs the entrance of glucose into the cells. However, glycogenolysis and gluconeogenesis increase the quantities of glucose available for glycolysis. In tissues with attendant vasoconstriction and diminished oxygen delivery the glucose cannot be completely metabolized by the tricarboxylic acid cycle, so that there is a shift from aerobic to a~aerobic metabolism. This is reflected in part by an increase of production of lactate relative to pyruvate (excess lactate) and thus to increased delivery of an acid load from the tissues. Furthermore, because of the difficulty of glucose entrance into cells and because of the overload of the glycolytic pathway, there is a transient "diabetic" response which is insulinresistant. Increased blood sugar after hemorrhage was first noted more than 100 years ago by Claude Bernard. Although it appears to have little significance of itself, it should be noted, however, that it indicates an inability of the tissues to remove glucose in a normal way. If glucose is administered in large amounts, blood concentration of this substance may be elevated and may overload renal reabsorptive mechanisms. PROTEIN METABOLISM. In most tissues, primarily as an effect of cortisol, decreased insulin, and decreased sex hormone secretion, the incorporation of amino acids into tissues is decreased. Since these tissues are normally in dynamic equilibrium, and since the movement of amino
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acids out of the cells is not impaired, there is a net catabolic effect. As nitrogen moves out of cells, potassium accompanies it, thus increasing the concentration of extracellular potassium relative to intracellular potassium. As noted above, this may impair muscular activity in striated muscle, smooth muscle, and cardiac muscle. The increased load of amino acids in turn is used primarily in gluconeogenesis as described above, and secondarily may be involved in the synthesis of new albumin. Increased quantities of albumin within the circulation act in turn by increasing onc otic pressure to hold within the vascular space fluid which has moved intravascularly across the capillaries from the extravascular extracellular fluid volume. FAT METABOLISM. The catecholamines, growth hormone, adrenocorticotropic hormone, and decreased insulin secretion all combine to increase the rate of lipolysis and the movement of fatty acids to the liver from peripheral tissues. The liver in turn synthesizes and releases lipoproteins. Whereas these elements are soluble in the blood in small quantities, when they are released in large amounts they may aggregate and form fat emboli, which may in turn impair pulmonary function. However, the overall effect of the metabolic response to injury is to increase the delivery of metabolic components for incorporation into the metabolic pathways which lead to formation of adenosine triphosphate, and for wound repair. Renal Response The primary response of the kidney to hemorrhage and trauma is the diminished excretion of salt and water. In severe injury, this may be produced by fall in the rate of glomerular filtration, but this is offset, initially at least, by an increase in tone within the efferent arterioles and possibly in addition by the action of cortisol. In the absence of renal failure, the diminished excretion of sodium and water is primarily the result of increased reabsorption of these substances from the proximal tubule, which is currently viewed as a decrease in "third factor." This "factor" appears to be a set of mechanisms which may involve a hormone which has thus far defied identification, but which appears to be primarily the result of increased peritubular oncotic pressure resulting from efferent arterial constriction and maintained glomerular filtration. In addition, the adrenal hormone aldosterone promotes the absorption of sodium and water from distal sites in the nephron and also facilitates the excretion of potassium and hydrogen ions. Furthermore, increased quantities of vasopressin within the circulation promote further reabsorption of water. The overall effect of the renal response to trauma is to prevent further depletion of blood volume, and thus secondarily to aid the restitution of that volume.
THERAPEUTIC IMPLICATIONS The overall body response to trauma outlined above has specific implications in the intensive care of the traumatized patient. In general we believe that the physician can act most effectively if he recognizes
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and attempts to support, in his therapeutic maneuvers, the attempt of the body to maintain effective circulation and oxygen delivery. However, he must be aware of limitations of functional reserve and of the existing mechanisms of response which have been engaged physiologically, in order to avoid overload of the system. For example, as a result of the renal response outlined above there is an inability to excrete large amounts of salt or water. Thus, even in the presence of relative depletion of body fluids, electrolyte solutions must be administered judiciously, with reference to actual losses (or displacements into "third space") in order to prevent circulatory overload and pulmonary edema. It should be noted, as Bartter has done, that the renal response to trauma resembles that to congestive heart failure, so that in patients with the combination of trauma and congestive failure, fluid therapy requires extreme care. The measurement of central venous pressure as an index of circulating volume has attracted enthusiastic support in recent years. However, this measurement may be misleading, according to the degree of vasoconstriction and of effectiveness of the myocardium. Similarly, although they may be extremely helpful adjuvants, fluid therapy must not be based solely upon volume and osmolality of the urine, but should be determined primarily by estimates of losses or translocations of fluid and by measurement of body weight. Since acidosis is a major result of hypoperfusion and vasoconstriction, and since a decrease in pH leads to decreased efficiency of contraction of muscle, efforts must proceed to correct this condition. In particular, the apparent alkalosis early in the post-traumatic period should not lull the physician into complacency, since it results from the combination of hyperventilation and diminished delivery of carbon dioxide from the tissues. If ventilatory effectiveness diminishes, and as restitution of blood volume leads to restored delivery of carbon dioxide and lactate from tissues, the alkalosis may shift rapidly to a profound metabolic acidosis. Intravenous administration of bicarbonate ion and maintenance of blood volume and thus of perfusion appear to be the best therapeutic measures at present. Since glucose cannot be metabolized normally after trauma, its infusion in large amounts may lead to additional loss of salt and water in the urine. Far from reflecting adequate fluid replacement, this response is merely an osmotic diuresis (it does reflect continued glomerular filtration) and will lead to increased deficits of fluid. Excess glucose administration is, therefore, to be avoided. Since glucose movement into cells is impaired and since this impairment is resistant to insulin, the use of glucose and insulin to treat the hyperkalemia of acidosis and injury is not as effective as in the case of renal failure. Again, the treatment of choice seems to be infusion of bicarbonate, which moves potassium into cells in exchange for hydrogen, unless the condition is severe enough to demand hemodialysis. Acute renal failure occasionally occurs as a result, perhaps, of increased filtration of free hemoglobin or myoglobin in the face of increased salt and water reabsorption. If high concentrations of pigment
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are detected early, there appears to be some protective effect of sustained osmotic diuresis. If this approach is selected, fluid depletion can be prevented by administration of mannitol in one-half isotonic saline. 4 Should full-blown renal failure occur, therapy should be directed to fluid restriction, with administration designed only to replace losses and to minimize catabolism. In calculating fluids to be administered, the water of oxidation of foodstuffs (endogenous as well as exogenous) must be considered. Measurement of body weight is of paramount importance. The availability of safe and early hemodialysis when renal failure occurs, and prevention of renal failure by early detection, volume replacement, and osmotic diuresis, has led to removal of renal failure as a common cause of death from trauma. In attempting to support the circulation, the physician must remember that prolonged vasoconstriction will increase acidosis and thus ultimately impair cardiac function itself. Accordingly, the primary support of peripheral circulation requires restitution of blood volume rather than vasoconstrictive drugs. However, it has been suggested that inotropic agents may be effective support, particularly in elderly patients, once circulating volume has been restored. Cardiac arrest is a common problem in the trauma patient. It is commonly preceded by hypoxia and acidosis, and may be prevented by proper attention to airway, oxygenation, and metabolism. The early use of lidocaine is indicated if evidence of myocardial irritability appears. If arrest or ventricular fibrillation occurs, it should be handled in the usual way by closed chest massage and defibrillation. Intracardiac administration of lidocaine, bicarbonate, isoproterenol, or occasionally calcium may prove a useful adjuvant to treatment. Support of oxygenation is of great importance, even in non-thoracic trauma. Assisted ventilation can improve distribution of gas within the lungs and diminish the frequency of atelectasis. Ventilatory support decreases the oxygen cost of breathing and thus can break the acidotic spiral. Increased end-expiratory pressure, as in continuous positive pressure breathing, can reduce the formation of pulmonary edema. The use of high concentrations of oxygen in inspired air may be required for brief periods, but prolonged administration of oxygen is to be avoided. If ventilation is supported and if atelectasis and pneumonitis are prevented, one can avoid the need for oxygen in many cases, but not in all (see below). A final complication which may arise as a direct result of the body response to trauma is the occurrence of stress ulceration of the stomach. Such lesions may result from a shunting of blood away from the gastric mucosa by prolonged nerve stimulation or from prolonged action of cortisol, with decreased resistance of the mucosa to acid. Some physicians suggest the use of prophylactic antacid therapy. If stress ulceration occurs, it commonly presents as bleeding, and is detected by hematemesis, melena, or deterioration of vital signs. Early diagnosis and treatment, conservative if possible, are imperative; if bleeding persists, gastric resection may be necessary.
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COMPLICATIONS OF TRAUMA The morbidity of trauma can be ascribed in part to the specific injury sustained and in part to three major kinds of complications. A major cause of death following trauma which appears to be increasing in importance is post-traumatic pulmonary insufficiency. This is a condition in which the lungs appear to be congested and there is interstitital edema, and in which the major physiologic evidence is de saturation of the arterial blood, even in the presence of high inspired tension of oxygen. It is generally associated with an increased rate of ventilation, and has been called "high-output respiratory failure."3 This phenomenon is poorly understood at present. It is measured as an increase in true shunt, or decrease in the ratio of ventilation to perfusion. However, many factors which may be the result of direct injury or the result of body response to trauma may play a role in the evolution of this complication. Some of these factors may be treated specifically and others may be prevented by early recognition. They include atelectasis, pulmonary edema, decreased ventilation, pneumonitis, bronchospasm, and decreased surfactant (a secondary complication of oxygen therapy). Therapeutic maneuvers which appear to be of some effectiveness are controlled respiration with continuous positive pressure breathing to elevate end-respiratory pressure and diminish edema production, antibiotics, maintenance of a patent airway, limited use of high oxygen tensions, and in certain instances, the use of bronchodilators. It appears increasingly, however, that this complication may result not only from tissue trauma and infection but may also result from the action of certain substances released into the bloodstream, which may include bradykinin, some of the prostaglandins (particularly prostaglandin F 2a ) and serotonin and histamine released from the breakup of platelet aggregates. However, these phenomena have not been well documented and their role is difficult to evaluate, so that therapy is at best empirical. In particular, as noted above, the use of high oxygen concentration in inspired air is unsatisfactory treatment, in part because it rarely increases to normal the degree of oxygen saturation in arterial blood and in part because it acts to destroy pulmonary surfactant. The possible role of new therapeutic maneuvers, such as oxygenation of the venous blood by partial bypass through a membrane oxygenator, is incompletely evaluated at this time. In general, the therapeutic approach to this complication depends upon early recognition and a direct approach to individual aggravating or preCipitating factors as they arise and are recognized. One may hope that therapy will improve as the process becomes better understood and as methods for early diagnosis are improved. The second major general complication of trauma during the period of intensive care is delayed hemorrhage. Hemorrhage may follow the lysis of a clot or the release of vasospasm. It is relatively common from the spleen, but may occur from other organs as well. Rarely it is the result of necrosis in a wound or a complication of initial surgical maneuver.
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Stress ulcer may also be the source of bleeding. The satisfactory treatment of hemorrhage depends upon its early recognition, direct maneuvers to control it, and adequate restitution of the blood volume, using fresh blood when necessary. A third major complication of trauma in general is infection. If tracheostomy or tracheal intubation has been done in order to maintain an airway or to support ventilation, a virulent form of tracheal bronchitis is relatively common, as is bronchopneumonia. If the bowel has been ruptured, or perforated, intraperitoneal gram-negative infection, peritonitis, and at times endotoxin shock may occur. The appropriate therapy of these infections as well as infections in wounds is evident and depends upon early recognition, the use of aseptic techniques to minimize contamination, particularly in the case of tracheostomy, the judicious use of antibiotics to meet specific bacterial complications, and in the case of endotoxin shock, early diagnosis and the supplementation of antibiotic therapy with massive doses of corticosteroids. The principle of surgical drainage of abscesses is essential, when such collections can be identified.
PATIENT MONITORING The preceding comments may be taken to imply that satisfactory intensive care of the trauma patient depends in part upon basing therapeutic decisions upon an integrated overall view of the behavior, physiologic compensation, and pathologic decompensation of the many organ systems within the body. In addition, therapeutic effectiveness will be increased only as it becomes possible to diagnose complications early, or even to predict the evolution of complications such as pulmonary insufficiency. One may hope that a better integrated view and earlier diagnosis may result from improved techniques of patient monitoring applied to these patients. The monitoring system for the traumatized patient must include the measurement of multiple respiratory functions and renal function as well as measures of circulatory effectiveness. In particular, the selection of the electrocardiogram as a primary monitored variable has little to recommend it, since cardiac derangement in cases of trauma is an exceedingly late sign of disturbance, and since this disturbance may reflect circulatory inadequacy, hypoxia, acidosis or hyperkalemia. Similarly, major reliance upon arterial pressure may provide the therapeutic team with only a late index of disturbance because of the many compensatory mechanisms which are activated by trauma and hemorrhage and which act, at least in major part, to maintain arterial pressure. At this time, there has been established no generally satisfactory monitoring system for the traumatized patient, though efforts are proceeding in this direction in a number of centers. The development of these systems depends, in turn, upon the development of monitoring systems which meet three criteria.
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First, attention must be directed to the measurement of appropriate variables, which include not only those which are most easily measured but those which are most commonly deranged, and among these, those in which derangements occur earliest. These include cardiovascular variables which are measured less commonly than is arterial pressure but which may reflect early changes which either trigger or signify compensatory action to maintain mean arterial pressure. These include arterial pulse pressure, maximum dP/dt, systolic ejection time, and cardiac output. Increased emphasis must be placed on respiratory variables, including blood gases, ventilatory flow, estimates of alveolar gas concentrations and, at times, esophageal (intrathoracic) pressure. With respect to renal function, one must observe not only the rate of urine flow but also sodium concentration, osmolality, and of course body weight. Since these variables differ in their dynamic properties, they need not all be measured with equal frequency. Rather, those variables which change fastest, such as some of the cardiovascular variables, must be measured as often as beat by beat, while certain respiratory variables change little over several hours, and so may be measured less often. Second, there are sets of variables which are not themselves measurable, but which may be computed from other measurable variables. An example of these is the computation of stroke volume from high quality pressure pulse tracings. Other computations include that of oxygen consumption as the integral of the product of oxygen concentration and air flow, which appears to be a sensitive index of incipient respiratory failure, as is the computation of oxygen cost of breathing which can be derived from oxygen consumption measured at different levels of airway resistance. Furthermore, lung compliance and resistance can be computed from a frequency analysis of pressure and flow,5 so that these variables can be made accessible without an inordinate degree of invasion of the patient. The availability of these computed variables at the bedside will permit evaluation of their utility in practice. However, preliminary observations suggest that the computed variables will be useful in providing physicians with earlier warning of derangements. Finally, work is just beginning to develop monitoring systems which evaluate the response of patients to small perturbations. This approach has been exceedingly useful in the evaluation of states of physical systems and holds high promise in the area of patient monitoring. In particular, such dynamic measurements can provide not only an index of performance but also an index of the reserve which remains in various organ systems. Perhaps the evolution of an ideal program for the intensive care of the trauma patient depends predominantly on further advances in this area.
REFERENCES 1. Bartter, F. C.: Cardiac failure and hormonal control of fluid and electrolyte balance. Surg. Gynec. Obstet., 118:767,1964. 2. Ballinger, W. F., 11, Rutherford, R. B., and Zuidema, G. D., eds.: The Management of Trauma. Philadelphia, W. B. Saunders, 1968.
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3. Burke, J. F., Pontoppidan, H., and Welch, C. E.: High output respiratory failure. Ann. Surg., 158:581,1963. 4. Gann, D. S., Wright, H. K., and Newsome, H. H.: Prevention of sodium depletion during osmotic diuresis. Surg. Gynec. Obstet., 119:265,1964. 5. Hilberman, M., Schill, J. P., and Peters, R. M.: On-line digital analysis of respiratory mechanics and the automation of respirator control. J. Thorac. Cardiovasc. Surg., 58:821,1969. 6. Moore, F. D., et al.: Post-Traumatic Pulmonary Insufficiency. Philadelphia, W. B. Saunders, 1969. 7. Shires, G. T., ed.: Care ofthe Trauma Patient. New York, McGraw-Hill, 1966. The Johns Hopkins University School of Medicine Baltimore, Maryland 21205