- Email: [email protected]
Differential diagnosis of hypovolemic shock
DifferentialDiagnosisof Hypovolemic Shock BENJAMIN
F. RUSH, JR., MD
The classic symptoms of hypovolemic shock have probably been recognized since prehistoric times. Clear, written descriptions did not emerge until the 19th century, and the syndrome implied impending, unpreventable death until the 20th century. We now have the tools for resuscitation of the large majority of patients in shock. When the shock syndrome is encountered in the field, away from the hospital and the emergency room, rapid transportation to these areas of more sophisticated diagnosis and treatment Is indicated.
Surely the violent life of primitive man, with its hunting accidents and tribal wars, must have made signs and symptoms of hemorrhagic shock familiar to the medicine men of many cultures long before the written word (Fig. 1). The Smith papyrus, inscribed over 4,000 years ago by an unknown Egyptian surgeon, is the first known surgical text. The 48 cases described there deal primarily with traumatic wounds and fractures of the head, neck, and chest. While a number of dramatic changes produced by injury of the brain and spinal cord are noted, no clear description of hemorrhagic shock appears. l Hippocrates,2 considered the father of Western medicine, wrote extensively of diagnosis, prognosis, and medical and surgical treatment. His writings reveal an extensive experience with wounds and fractures, but he likewise failed to leave a clear picture of the signs or symptoms of shock and trauma, except possibly in his aphorisms. In the first aphorism of the seventh section, he notes “In acute diseases coldness of the extremities is bad,” and in the ninth aphorism of the same section, “Delirium or convulsion from a flow of blood is bad.” Soranus3 of Ephesus, a Greek physician who studied at Alexandria and practiced in Rome in the first century A.D., wrote extensively of various diseases, but there is no clear description of hemorrhage related to the shock syndrome. There is an interesting passage in his section on apoplexy, in which he defines a form of From the Department of Surgery, UMDNJ, New Jersey Medical School, Newark, New Jersey. Presented at the First International Conference on the Basic Mechanisms and Clinical Management of Shock, Merrillville, Indiana, September 10-11, 1982, and accepted for publication at that time. Address reprint requests to Dr. Rush: Department of Surgery, UMDNJ, New Jersey Medical School, 100 Bergen Avenue, Newark, NJ 07103. Key Words: Hypovolemia, shock. 82
apoplexy without fever or paralysis which “strikes suddenly-the pulse is rapid as if fleeing from pursuit-limbs cold and numb, respiration smal1 and complexion leaden-if the disease tends towards a fatal conclusion-the patient’s face is drawn, cold, numbness of the whole body-cold sweat in the upper parts.” The description certainly suggests a patient with occult, extensive fluid loss. Also in the first century A.D., Celsus4 wrote of wounds of the heart: “When the heart is penetrated much blood issues, the pulse fades away, the color is extremely pallid, cold and malodorous sweat bursts out as if the body has been wetted by dew. The extremities become cold and death follows quickly.” The ultimate experts in wounds of the heart were the Aztec and Mayan priests, who expertly split the sternum of their victims with a sacrificial knife, jerked the heart from the thorax, and held it up to be viewed by the worshiping congregation. The longer the heart continued to beat, the more auspicious were the signs.5 The changes wrought in the heartless body were of little interest, and no descriptions of it were left. The artists of the Renaissance showed varying appreciation of the effects of trauma. Castagno’s St. Sebastian (UI. 1457) looks mildly annoyed by his many wounds. In Terbrugghen’s depiction of the crucifixion (ca. 1600), Christ shows clear evidence of shock. The first surgical text ever written in English (1597) was “The Whole Course of Chirugerie” by Lowe,h an engaging and enormously experienced Scats surgeon whose great depth of knowledge was developed during his service as military surgeon to Flemish. French, and Spanish kings on the continent for many years, as well as in an interesting episode as a pirate raiding the English fleet. In the section “Mortal Wounds” of Lowe’s text, we find a passage not unlike the one from Celsus, but embellished with a few realistic details: “We know the heart to be hurt when there cometh out quantitie of blood, thick and black chiefly if the right side be hurt, if the left, it is more red and subtill (sic), trembling, casting a cold ill-favored sweat, the extremities waxed cold, often sounding, and dieth shortly.” These last two passages from Lowe and Celsus are certainly a clear description of the shock syndrome progressing rapidly toward death. It is probable that many of the ancient scribes who wrote of surgical treatment were so familiar with this sequence of events and so well aware that a patient with such mortal signs and symp-
RUSH W HYPOVOLEMIC
SHOCK
FIGURE 1. Cave painting from Lascaux, France (ca. lS,OOO10,000 B.C.). The wounded and apparently eviscerated bison stands over the wounded or dead hunter. An example of the violent life of primitive man.
toms would not come to therapy that they did not find it necessary to write of such things. If shock is defined as a failure of adequate tissue perfusion, a host of conditions can bring it about. Most commonly, there is either a failure of the pump (cardiogenic shock) or a failure of volume return to the heart. The latter state can occur because of loss of circulatory volume (hemorrhage; dehydration; capillary leak of fluids, as in burns and trauma) or from sudden dilatation of the vascular space (neurogenic shock). The problem of diagnosing shock may be encountered at locations with different levels of sophistication: in the field, in the emergency room, or, with the most resources available, in the operating room or intensive care unit.
FIELDDIAGNOSIS The major task when patients are seen in the field is to recognize that they are in shock and promptly remove them to a hospital. The only tools available are usually a knowledge of the precipitating event (trauma, sudden chest pain, etc.), the vital signs, and the general appearance of the patient. Concerns about differential diagnosis and etiology are postponed until the patient arrives at the emergency room. In the first chapter of his book on traumatic shock, Cannon7 quotes two beautiful descriptions of the signs engendered by hemorrhagic shock. In both of these cases, the amount of bleeding was minimal, and Cannon was reflecting the puzzlement of scientists of his day in finding this syndrome in patients who did
not appear to have lost blood. As the work of Blalock8 and Parsons and Phemister9 was soon to demonstrate, the presence of such signs in traumatized patients do indeed reflect hypovolemic shock from occult loss of blood and plasma into the tissues. In any case, these descriptions remain as classic examples of the shock syndrome provoked by hemorrhage. The first was by Fischer, a German surgeon, whose description was published in 1870: the patient a strong and perfectly healthy young man was
struck in the abdomen by the pole of a carriage drawn by run-away horses. We have not been able after careful examination to find any trace of injury to any of the internal organs. Nevertheless, the grave symptoms and the alarming look which he still presents made their appearance immediately after the accident. He lies perfectly quiet and pays no attention whatever to events about him. The pupils are dilated and react slowly to light. He stares purposelessly and apathetically straight before him. His skin and such parts of the mucous membranes as are visible are as pale as marble, and his hands and lips have a bluish tinge. Large drops of sweat hang on his forehead and eyebrows, his whole body feels cold to the hand, and a thermometer indicates a degree and a half centigrade in the axillae and a degree in the rectum, below the normal. Sensibility is much blunted over the whole body, and only when a very painful impression is made on the patient does he fretfully pull a wry face and make a languid defensive movement. If the limbs are lifted and then left go, they immediately fall as if dead. The urine is scanty and dense, but free from any traces of sugar and albumin. The pulse is almost imperceptible and very rapid. The arteries are small and the tension very low. The patient is conscious, but replies slowly and only when repeatedly 83
AMERICAN
JOURNAL
OF EMERGENCY
MEDICINE
m Volume 2, Number 1
consider the patient to be in severe agonal shock (Fig. 2). Lesser degrees of shock would be reflected by clearer mentation and an obtainable systolic blood pressure between 50 and 70 mm Hg. Even milder shock is reflected by a systolic and a diastolic pressure between 70 and 90 mm Hg and a pulse no greater than 120 beats/min. Blood pressure and pulse only reflect the momentary state. If the observed blood loss or extent of trauma suggests that the patient should be in severe shock, the observor should treat the patient accordingly and not be taken by surprise by a sudden deterioration in the patient’s condition (Fig. 3). Champion and othersi have proposed a simple physiologic index to permit personnel in the field to quickly assess the severity of trauma. Points are allocated to the various physiologic parameters, and the additive score obtained is the “trauma index,” which can be correlated with the probable mortality. By this method, Fischer’s patient would score about 9, with a probable mortality rate of 63%.
dilated pupils languid expression
cold sweat
gasping respiration
pallid complexion
FIGURE 2. Classic signs of hypovolemic shock. Any condition that severely impairs tissue perfusion may elicit similar signs, i.e., cardiac failure or sepsis. and importunely
questioned. On being thus questioned, he complains of cold, faintness and deadness of the extremities. His respiration is characterized by long, deep, sighing in-
spirations alternating with very superficial ones which are scarcely visable or audible. While being brought to the hospital, he vomited several times and nausea and hiccups still remain. His pallor, cold skin and hoarse voice immediately recalls the appearance of a cholera patient; characteristic dejections are alone wanting to make the resemblance complete .
EMERGENCY DEPARTMENT DIAGNOSIS In the emergency room, much more sophisticated tools for diagnosing the patient’s state are available. Electrocardiographic monitoring warns against cardiac irregularity and possible sudden cardiac arrest. Blood for baseline hematocrits can be drawn as resuscitation begins. A search for occult bleeding by peritoneal lavage or thorocentesis is done as indicated. Determination of blood pH, and especially lactate concentration, can help to determine the severity and length of shock. Two of the most useful diagnostic tests in deter-
The other case that Cannon quotes is by Warren, in 1885, concerning a patient with a compound comminuted fracture where “the bleeding has been slight.” Certainly any physician or paramedic presented “in the street” with the picture just described, together with (probably) an unobtainable blood pressure, would
SYSTOLIC B.l?
1150 PULSE
VOLUME LOSS
FIGURE 3. Response of blood pressure and pulse to blood loss. Vital signs may not immediately indicate the severity of blood loss, depending on how rapid the loss has been and how much time there has been for compensation. At least one third of the total blood volume must be lost for a persistent hypotension to be produced.
60 -+’
80 -
- 30 BLEEDING STARTS t
100
0
15
I
I
I
I
30
45
60
75
TIME
84
9:
RUSH n HYPOVOLEMIC
mining the kind and degree of shock appearing in patients in the emergency department are the central venous pressure (CVP) and the test infusion. A high CVP accompanied by a low blood pressure usually implicates the heart as the source of trouble. A low CVP implies a peripheral vascular problem. In the latter case, rapid infusion of two liters of Ringer’s lactate or another balanced electrolyte solution will help to differentiate neurogenic from severe hypovolemic shock, and the change in the hematocrit from the baseline value will help to indicate the amount of blood lost. Until transfusions are started, the patient’s hematocrit maintains a relationship to the loss of erythrocyte mass as fluids are administered. If the vital signs become stable and CVP rises into the normal range, the difference between the baseline hematocrit and the final hematocrit will be a fairly accurate indicator of lost erythrocyte mass.” So many accidents are related to alcohol or drugs that the possible role of these agents must be considered in patients in shock. This is especially true when the severity of the hypotension seems to exceed the severity of the apparent injuries. Blood alcohol levels should be obtained; if there is any suspicion of narcotic use, a test dose of a narcotic antagonist should be given. When hypotension is mainly due to intoxication, the blood pressure usually responds well to an infusion of electrolyte solution. A catheter in the patient’s bladder not only serves to detect renal or bladder injury but also is basic to determining the adequacy of tissue perfusion. If urinary output can be measured at 50 ml/h or more, reasonably adequate tissue perfusion can be assumed.
DIAGNOSIS IN THE INTENSIVE CARE UNIT All of the techniques begun in the emergency room are continued in the intensive care unit. Insertion of a Swan-Ganz catheter permits careful measurements of pulmonary artery and wedge pressures, pulse, cardiac output, and all of the derived values for pulmonary and cardiac function, making the most precise determinations of the patient’s condition possible. It is a grievous error to treat a patient with diminished urinary output and a low right heart pressure with diuretics. Until the vascular space is clearly filled, as indicated by normal or high normal right
SHOCK
heart pressures, any evidence of lowered renal output is clearly related to the continuing poor perfusion of the kidneys. Diuretics will only make the situation worse. Such powerful diuretics as ethacrynic acid and furosemide will, in fact, force the kidneys to excrete additional urine even in the presence of a decreased vascular load, making the patient’s condition even more desperate.
DIAGNOSIS OF SEPTIC SHOCK Septic shock usually does not become a problem in differential diagnosis until the third to fourth day after injury or even later. A rising temperature with a sudden or sometimes a gradual drop in blood pressure suggests septic shock. If the cardiac output as measured through the Swan-Ganz catheter is rising, this confirms septic shock. If the clinical picture suggests septic shock but cardiac output falls, there may be more than one cause. Hypovolemic shock may coexist with septic shock and requires fluid replacement until the cardiac output begins to rise above normal.
REFERENCES 1. Bresled JH. Edwin Smith Papyrus (translation). NY Sot 0 Bull April 1922. 2. Adams F. The Genuine Works of Hippocrates. New York: Wm Woods & Co, 1929. 3. Drabkin IE. (Caelius Aurelianus, translator.) Soranus of Ephesus on Acute Diseases and Chronic Diseases. Chicago: University of Chicago Press, 1950. 4. Celsus. (WG Spencer, translator.) De Medicina. Cambridge: Harvard University Press, 1960. 5. Leake CD. The historic development of cardiovascular physiology. In Hamilton WF, Dow P. Circulation, Section 2. Washington: American Physiological Society, 1962. 6. Lowe P. The Whole Course of Chirurgerie. London: Thomas Purfoot, 1597. 7. Cannon WB. Traumatic Shock. New York: DW Appleton, 1923. 8. Blalock H. Experimental Shock: The cause of low blood pessure produced by muscle injury. Arch Surg 1930;20:959. 9. Parsons E, Phemister DB. Hemorrhage and “shock” in traumatized limbs. Surg Gynecol Obstet 1930;51:196. 10. Champion HR, Sacco WJ, Carnazzo AJ, et al. Trauma Score. Crit Care Med 1961;9:672. 11. Rush BF. Volume replacement: When, what and how much? In Schumer W, Nyhus LM (eds). Treatment of Shock: Principles and Practice. Philadelphia. Lea & Febiger, 1974.
85
F. RUSH, JR., MD
The classic symptoms of hypovolemic shock have probably been recognized since prehistoric times. Clear, written descriptions did not emerge until the 19th century, and the syndrome implied impending, unpreventable death until the 20th century. We now have the tools for resuscitation of the large majority of patients in shock. When the shock syndrome is encountered in the field, away from the hospital and the emergency room, rapid transportation to these areas of more sophisticated diagnosis and treatment Is indicated.
Surely the violent life of primitive man, with its hunting accidents and tribal wars, must have made signs and symptoms of hemorrhagic shock familiar to the medicine men of many cultures long before the written word (Fig. 1). The Smith papyrus, inscribed over 4,000 years ago by an unknown Egyptian surgeon, is the first known surgical text. The 48 cases described there deal primarily with traumatic wounds and fractures of the head, neck, and chest. While a number of dramatic changes produced by injury of the brain and spinal cord are noted, no clear description of hemorrhagic shock appears. l Hippocrates,2 considered the father of Western medicine, wrote extensively of diagnosis, prognosis, and medical and surgical treatment. His writings reveal an extensive experience with wounds and fractures, but he likewise failed to leave a clear picture of the signs or symptoms of shock and trauma, except possibly in his aphorisms. In the first aphorism of the seventh section, he notes “In acute diseases coldness of the extremities is bad,” and in the ninth aphorism of the same section, “Delirium or convulsion from a flow of blood is bad.” Soranus3 of Ephesus, a Greek physician who studied at Alexandria and practiced in Rome in the first century A.D., wrote extensively of various diseases, but there is no clear description of hemorrhage related to the shock syndrome. There is an interesting passage in his section on apoplexy, in which he defines a form of From the Department of Surgery, UMDNJ, New Jersey Medical School, Newark, New Jersey. Presented at the First International Conference on the Basic Mechanisms and Clinical Management of Shock, Merrillville, Indiana, September 10-11, 1982, and accepted for publication at that time. Address reprint requests to Dr. Rush: Department of Surgery, UMDNJ, New Jersey Medical School, 100 Bergen Avenue, Newark, NJ 07103. Key Words: Hypovolemia, shock. 82
apoplexy without fever or paralysis which “strikes suddenly-the pulse is rapid as if fleeing from pursuit-limbs cold and numb, respiration smal1 and complexion leaden-if the disease tends towards a fatal conclusion-the patient’s face is drawn, cold, numbness of the whole body-cold sweat in the upper parts.” The description certainly suggests a patient with occult, extensive fluid loss. Also in the first century A.D., Celsus4 wrote of wounds of the heart: “When the heart is penetrated much blood issues, the pulse fades away, the color is extremely pallid, cold and malodorous sweat bursts out as if the body has been wetted by dew. The extremities become cold and death follows quickly.” The ultimate experts in wounds of the heart were the Aztec and Mayan priests, who expertly split the sternum of their victims with a sacrificial knife, jerked the heart from the thorax, and held it up to be viewed by the worshiping congregation. The longer the heart continued to beat, the more auspicious were the signs.5 The changes wrought in the heartless body were of little interest, and no descriptions of it were left. The artists of the Renaissance showed varying appreciation of the effects of trauma. Castagno’s St. Sebastian (UI. 1457) looks mildly annoyed by his many wounds. In Terbrugghen’s depiction of the crucifixion (ca. 1600), Christ shows clear evidence of shock. The first surgical text ever written in English (1597) was “The Whole Course of Chirugerie” by Lowe,h an engaging and enormously experienced Scats surgeon whose great depth of knowledge was developed during his service as military surgeon to Flemish. French, and Spanish kings on the continent for many years, as well as in an interesting episode as a pirate raiding the English fleet. In the section “Mortal Wounds” of Lowe’s text, we find a passage not unlike the one from Celsus, but embellished with a few realistic details: “We know the heart to be hurt when there cometh out quantitie of blood, thick and black chiefly if the right side be hurt, if the left, it is more red and subtill (sic), trembling, casting a cold ill-favored sweat, the extremities waxed cold, often sounding, and dieth shortly.” These last two passages from Lowe and Celsus are certainly a clear description of the shock syndrome progressing rapidly toward death. It is probable that many of the ancient scribes who wrote of surgical treatment were so familiar with this sequence of events and so well aware that a patient with such mortal signs and symp-
RUSH W HYPOVOLEMIC
SHOCK
FIGURE 1. Cave painting from Lascaux, France (ca. lS,OOO10,000 B.C.). The wounded and apparently eviscerated bison stands over the wounded or dead hunter. An example of the violent life of primitive man.
toms would not come to therapy that they did not find it necessary to write of such things. If shock is defined as a failure of adequate tissue perfusion, a host of conditions can bring it about. Most commonly, there is either a failure of the pump (cardiogenic shock) or a failure of volume return to the heart. The latter state can occur because of loss of circulatory volume (hemorrhage; dehydration; capillary leak of fluids, as in burns and trauma) or from sudden dilatation of the vascular space (neurogenic shock). The problem of diagnosing shock may be encountered at locations with different levels of sophistication: in the field, in the emergency room, or, with the most resources available, in the operating room or intensive care unit.
FIELDDIAGNOSIS The major task when patients are seen in the field is to recognize that they are in shock and promptly remove them to a hospital. The only tools available are usually a knowledge of the precipitating event (trauma, sudden chest pain, etc.), the vital signs, and the general appearance of the patient. Concerns about differential diagnosis and etiology are postponed until the patient arrives at the emergency room. In the first chapter of his book on traumatic shock, Cannon7 quotes two beautiful descriptions of the signs engendered by hemorrhagic shock. In both of these cases, the amount of bleeding was minimal, and Cannon was reflecting the puzzlement of scientists of his day in finding this syndrome in patients who did
not appear to have lost blood. As the work of Blalock8 and Parsons and Phemister9 was soon to demonstrate, the presence of such signs in traumatized patients do indeed reflect hypovolemic shock from occult loss of blood and plasma into the tissues. In any case, these descriptions remain as classic examples of the shock syndrome provoked by hemorrhage. The first was by Fischer, a German surgeon, whose description was published in 1870: the patient a strong and perfectly healthy young man was
struck in the abdomen by the pole of a carriage drawn by run-away horses. We have not been able after careful examination to find any trace of injury to any of the internal organs. Nevertheless, the grave symptoms and the alarming look which he still presents made their appearance immediately after the accident. He lies perfectly quiet and pays no attention whatever to events about him. The pupils are dilated and react slowly to light. He stares purposelessly and apathetically straight before him. His skin and such parts of the mucous membranes as are visible are as pale as marble, and his hands and lips have a bluish tinge. Large drops of sweat hang on his forehead and eyebrows, his whole body feels cold to the hand, and a thermometer indicates a degree and a half centigrade in the axillae and a degree in the rectum, below the normal. Sensibility is much blunted over the whole body, and only when a very painful impression is made on the patient does he fretfully pull a wry face and make a languid defensive movement. If the limbs are lifted and then left go, they immediately fall as if dead. The urine is scanty and dense, but free from any traces of sugar and albumin. The pulse is almost imperceptible and very rapid. The arteries are small and the tension very low. The patient is conscious, but replies slowly and only when repeatedly 83
AMERICAN
JOURNAL
OF EMERGENCY
MEDICINE
m Volume 2, Number 1
consider the patient to be in severe agonal shock (Fig. 2). Lesser degrees of shock would be reflected by clearer mentation and an obtainable systolic blood pressure between 50 and 70 mm Hg. Even milder shock is reflected by a systolic and a diastolic pressure between 70 and 90 mm Hg and a pulse no greater than 120 beats/min. Blood pressure and pulse only reflect the momentary state. If the observed blood loss or extent of trauma suggests that the patient should be in severe shock, the observor should treat the patient accordingly and not be taken by surprise by a sudden deterioration in the patient’s condition (Fig. 3). Champion and othersi have proposed a simple physiologic index to permit personnel in the field to quickly assess the severity of trauma. Points are allocated to the various physiologic parameters, and the additive score obtained is the “trauma index,” which can be correlated with the probable mortality. By this method, Fischer’s patient would score about 9, with a probable mortality rate of 63%.
dilated pupils languid expression
cold sweat
gasping respiration
pallid complexion
FIGURE 2. Classic signs of hypovolemic shock. Any condition that severely impairs tissue perfusion may elicit similar signs, i.e., cardiac failure or sepsis. and importunely
questioned. On being thus questioned, he complains of cold, faintness and deadness of the extremities. His respiration is characterized by long, deep, sighing in-
spirations alternating with very superficial ones which are scarcely visable or audible. While being brought to the hospital, he vomited several times and nausea and hiccups still remain. His pallor, cold skin and hoarse voice immediately recalls the appearance of a cholera patient; characteristic dejections are alone wanting to make the resemblance complete .
EMERGENCY DEPARTMENT DIAGNOSIS In the emergency room, much more sophisticated tools for diagnosing the patient’s state are available. Electrocardiographic monitoring warns against cardiac irregularity and possible sudden cardiac arrest. Blood for baseline hematocrits can be drawn as resuscitation begins. A search for occult bleeding by peritoneal lavage or thorocentesis is done as indicated. Determination of blood pH, and especially lactate concentration, can help to determine the severity and length of shock. Two of the most useful diagnostic tests in deter-
The other case that Cannon quotes is by Warren, in 1885, concerning a patient with a compound comminuted fracture where “the bleeding has been slight.” Certainly any physician or paramedic presented “in the street” with the picture just described, together with (probably) an unobtainable blood pressure, would
SYSTOLIC B.l?
1150 PULSE
VOLUME LOSS
FIGURE 3. Response of blood pressure and pulse to blood loss. Vital signs may not immediately indicate the severity of blood loss, depending on how rapid the loss has been and how much time there has been for compensation. At least one third of the total blood volume must be lost for a persistent hypotension to be produced.
60 -+’
80 -
- 30 BLEEDING STARTS t
100
0
15
I
I
I
I
30
45
60
75
TIME
84
9:
RUSH n HYPOVOLEMIC
mining the kind and degree of shock appearing in patients in the emergency department are the central venous pressure (CVP) and the test infusion. A high CVP accompanied by a low blood pressure usually implicates the heart as the source of trouble. A low CVP implies a peripheral vascular problem. In the latter case, rapid infusion of two liters of Ringer’s lactate or another balanced electrolyte solution will help to differentiate neurogenic from severe hypovolemic shock, and the change in the hematocrit from the baseline value will help to indicate the amount of blood lost. Until transfusions are started, the patient’s hematocrit maintains a relationship to the loss of erythrocyte mass as fluids are administered. If the vital signs become stable and CVP rises into the normal range, the difference between the baseline hematocrit and the final hematocrit will be a fairly accurate indicator of lost erythrocyte mass.” So many accidents are related to alcohol or drugs that the possible role of these agents must be considered in patients in shock. This is especially true when the severity of the hypotension seems to exceed the severity of the apparent injuries. Blood alcohol levels should be obtained; if there is any suspicion of narcotic use, a test dose of a narcotic antagonist should be given. When hypotension is mainly due to intoxication, the blood pressure usually responds well to an infusion of electrolyte solution. A catheter in the patient’s bladder not only serves to detect renal or bladder injury but also is basic to determining the adequacy of tissue perfusion. If urinary output can be measured at 50 ml/h or more, reasonably adequate tissue perfusion can be assumed.
DIAGNOSIS IN THE INTENSIVE CARE UNIT All of the techniques begun in the emergency room are continued in the intensive care unit. Insertion of a Swan-Ganz catheter permits careful measurements of pulmonary artery and wedge pressures, pulse, cardiac output, and all of the derived values for pulmonary and cardiac function, making the most precise determinations of the patient’s condition possible. It is a grievous error to treat a patient with diminished urinary output and a low right heart pressure with diuretics. Until the vascular space is clearly filled, as indicated by normal or high normal right
SHOCK
heart pressures, any evidence of lowered renal output is clearly related to the continuing poor perfusion of the kidneys. Diuretics will only make the situation worse. Such powerful diuretics as ethacrynic acid and furosemide will, in fact, force the kidneys to excrete additional urine even in the presence of a decreased vascular load, making the patient’s condition even more desperate.
DIAGNOSIS OF SEPTIC SHOCK Septic shock usually does not become a problem in differential diagnosis until the third to fourth day after injury or even later. A rising temperature with a sudden or sometimes a gradual drop in blood pressure suggests septic shock. If the cardiac output as measured through the Swan-Ganz catheter is rising, this confirms septic shock. If the clinical picture suggests septic shock but cardiac output falls, there may be more than one cause. Hypovolemic shock may coexist with septic shock and requires fluid replacement until the cardiac output begins to rise above normal.
REFERENCES 1. Bresled JH. Edwin Smith Papyrus (translation). NY Sot 0 Bull April 1922. 2. Adams F. The Genuine Works of Hippocrates. New York: Wm Woods & Co, 1929. 3. Drabkin IE. (Caelius Aurelianus, translator.) Soranus of Ephesus on Acute Diseases and Chronic Diseases. Chicago: University of Chicago Press, 1950. 4. Celsus. (WG Spencer, translator.) De Medicina. Cambridge: Harvard University Press, 1960. 5. Leake CD. The historic development of cardiovascular physiology. In Hamilton WF, Dow P. Circulation, Section 2. Washington: American Physiological Society, 1962. 6. Lowe P. The Whole Course of Chirurgerie. London: Thomas Purfoot, 1597. 7. Cannon WB. Traumatic Shock. New York: DW Appleton, 1923. 8. Blalock H. Experimental Shock: The cause of low blood pessure produced by muscle injury. Arch Surg 1930;20:959. 9. Parsons E, Phemister DB. Hemorrhage and “shock” in traumatized limbs. Surg Gynecol Obstet 1930;51:196. 10. Champion HR, Sacco WJ, Carnazzo AJ, et al. Trauma Score. Crit Care Med 1961;9:672. 11. Rush BF. Volume replacement: When, what and how much? In Schumer W, Nyhus LM (eds). Treatment of Shock: Principles and Practice. Philadelphia. Lea & Febiger, 1974.
85