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Study of Fifth U. S. Army Hospital Battle Casualty Deaths1
Howard E. Snyder, M.D., and James W. Culbertson, M.D.
From 1 January 1944 until the surrender of the German armies in Italy on 2 May 1945 (the period covered in this study), 91,631 American soldiers serving in the Fifth U.S. Army were killed or wounded in action (table 120). Of this total, 16,648 (18.2 percent) died on the battlefield or before reaching a medical installation; 11,959 (13 percent) were treated and returned to duty from the division area (fig. 258). Of the remaining 63,024 (68.8 percent) who were admitted to Fifth U.S. Army hospitals (fig. 259), only 1,631 (1.8 percent) died after their admission. Records of 1,411 (86.47 percent) of these hospital battle casualty deaths were available for this study. In addition, the records of 39 casualties who were DOA (dead on arrival) at a hospital were utilized in many sections of this report. Gross post mortem findings formed a part of 733 of these records (table 121). Microscopic autopsy reports were received on 349. Most of the clinical records were fairly complete,
but, in some, much desirable information was missing. However, most of the autopsies were performed by the operating surgeons already engaged in the arduous surgical tasks associated with an offensive, and the records are a tribute to the scientific zeal of the surgeons working in the Fifth U.S. Army hospitals.
1Includes records of 39 casualties who were DOA at a hospital.
It may be assumed that the 1,411 hospital battle casualty deaths studied are truly representative of the total of 1,631 who (according to MTOUSA MD Form 86f) died in Fifth U.S. Army hospitals. Beginning with 1 January 1944, General Martin requested submission of a complete record on all battle casualties dying in Fifth U.S. Army hospitals. From 1 January 1944 to 2 May 1945, the Adjutant General's "Wound Classification Report" submitted by the hospitals listed 58,677 battle casualty admissions and 1,562 battle casualty deaths in hospitals. These figures are lower than those reported on the MTOUSA MD Form 86f. From the latter, the figure for battle casualty hospital admissions is 63,024 and for battle casualty hospital deaths, 1,631. These larger figures have been used in setting 86.5 percent as the portion studied of all the hospital battle casualty deaths and have been correspondingly reduced when calculating percentage mortalities. In calculating percentages of total battle casualties or of battle casualty hospital admissions, by period, correction has been made for the percentage of cases studied during each period (table 122).
The Adjutant General's figures and the MTOUSA MD Form 86f include the injured in action as well as the WIA and the KIA casualties. Of the deaths studied, only a few who had crush injuries might be regarded as injured rather than as wounded in action. All of the casualties (20) due to crush injuries resulted from falling stones or bricks set in motion by the explosion of
1Data obtained from MTOUSA MD Form 86f.
an enemy shell, and most of these casualties had wounds in addition to the crush injury. It may be said, then, that the deaths studied represent a considerably larger percentage of WIA casualties who died than is indicated by the percentage of 86.5 percent which is based upon the total (1,631) of wounded and injured in action who died in Fifth U.S. Army hospitals during the period studied. The breakdown of injured in action and wounded in action is not available either for hospital battle casualty admissions or for the total resulting from the sum of the Adjutant General's figures on wounded in action plus killed in action.
The 39 records of battle casualties DOA at a hospital comprise all the records submitted on this class of deaths. Statistics are not available to determine their percentage of the entire group of DOA's. Most of them were unquestionably patients who, when seen by the last medical officer, were expected to reach the hospital alive. The DOA group has been included in the tables on wound classification and causes of death and, in many instances, has been singled out for individual study as compared to the group of casualties who died shortly after admission, before anesthesia, during anesthetic induction, during primary surgery, and after primary surgery. The cases have not been included in tables dealing with hospital battle casualty deaths or in any of the percentage tables based on hospital battle casualty admissions or the total of wounded in action plus killed in action.
The information recorded in the tables of this report was first recorded in code form so that it might be transferred to machine records cards. Study of the cases and the primary recording of these data consumed the entire time of Capt. (later Maj.) James W. Culbertson, MC, (fig. 260), for a period of a little
over 3 months. Col. Howard E. Snyder, MC, (fig. 261) then studied each case and checked the recorded data.2 Each item was carefully weighed, matters calling for opinion were discussed, and all questionable data were recorded as questionable. The completed machine records cards were checked by hand for accuracy. Colonel Snyder and Captain Culbertson, with their clerical assistants, did all machine counting and recording of data. Many checks were made on the validity of the machine tabulations. It is considered that the margin of error in this method was no greater than, if as great as, the personal error in manual counting.
REGION, TYPE, AND DISTRIBUTION OF WOUNDS
Table 123 lists the general breakdown of the 1,450 casualties as related to hospital admission, anesthesia, and surgery. With experience and improvement in the preparation of battle casualties for surgery, the number of those dying before anesthesia decreased throughout the period covered in the report. When one compares the distribution of hospital deaths during the various time
periods to the total hospital battle casualty admissions (table 124), there is a consistent reduction in the percentage of those dying before, during, and after anesthesia. Casualties at the Anzio beachhead were included in the first two periods of the survey (January-March 1944; April-July 1944) and unquestionably increased the percentage of those dying before anesthesia and the total hospital battle casualty mortality in the first two periods. The reduction in the latter mortality figure from 3.9 percent in the first period to 2.0 percent in the last is dependent on more than the Anzio casualties. The reduction in the percentage of those dying before anesthesia is in part due to the general adoption of improved methods of resuscitation and to a more available supply of blood. A hospital battle casualty mortality rate is influenced not only by the hospital's proximity to the battlefront but also by the quality of care administered the wounded who reach it alive.
Morrissey has called attention to the direct relationship of the percentage mortality of battle casualties admitted to hospitals, the percentage mortality of battle casualties admitted to hospitals and dying before anesthesia, and the percentage hospital battle casualty deaths comprised of the total who die of wounds (includes KIA) (table 125). He has shown that the latter percentage varies widely. At Anzio, 16 percent of all battle casualty deaths occurred in hos-
1Excludes 39 DOA casualties. Their
distribution was as follows: For the January-March 1944 period, 7; for
April-July 1944, 16; for August-December 1944, 16; for August-December 1944, 9;
and for January-May 1945, 7.
1Excludes 39 DOA casualties.
pitals (hospital mortality, 5.7 percent). In May 1944, 4.21 percent of all battle casualty deaths occurred in hospitals (hospital mortality, 1.7 percent). In June 1944, 15 percent of all battle casualty deaths were in hospitals (hospital mortality, 2.8 percent). In October 1944, 7.65 percent of all battle casualty deaths were in hospitals (hospital mortality, 2.1 percent). When evacuation of the wounded to the forward hospital (fig. 262) is easily accomplished,
the hospital mortality rises. Thus, hospital mortality tends to vary inversely with the percentage who are killed in action or who die of wounds before reaching a hospital. However, as is shown in table 125, there has been a steady, gradual decrease in the percentage which deaths occurring during and after surgery comprise of total battle casualty deaths. Table 124 shows a slight increase throughout the four periods in the percentage which deaths during surgery comprise of the deaths studied but a decrease in the percentage these deaths comprise of battle casualties admitted to hospitals.
The simple classification of cases by region of principal wound in table 126 is presented for comparison with similar tables on hospital battle casualty admissions and deaths which were available for all of the Tunisian, Sicilian, and Italian campaigns.
Table 127 lists battle casualty hospital deaths according to principal wound groups. It was found that in only 33.3 percent of the casualties studied were the wounds limited to one of the wound groups listed in this table, and 66.7 percent of the casualties had wounds involving multiple regions of the body. Many of the 33.3 percent had multiple wounds, but these wounds were limited to only one of the anatomic regions.3
TABLE 125.-Demonstration of effect of increased efficiency of evacuation from forward areas on hospital mortality (an increase) and the remaining favorable trend after exclusion of those cases1 dying before anesthesia
1A variable quantity influenced by
conditions affecting efficiency of evacuation to hospitals as well as by
professional care before and after admission.
Table 127 may be compared with the distribution of wounds among all battle casualties admitted to Fifth U.S. Army hospitals during the period of 1 August 1944 to 2 May 1945 (table 128). Intra-abdominal wounds comprise only 2.84 percent of battle casualties admitted to a hospital but 20 percent of them died and these comprise 28.1 percent of all hospital battle casualty deaths.
1A more detailed classification is
listed in appendix D, p. 807.
NOTE.-0.0 indicates a rate of more than zero but less than 0.05, and 0.00 a rate of more than zero but less than 0.005.
The intra-abdominal, intrathoracic, thoracoabdominal, combined intra-abdominal and intrathoracic, and intracranial wounds comprise only 11.09 percent of hospital battle casualty admissions, and yet they account for 76.8 percent of all hospital battle casualty deaths. Table 129 relates the 1,411 hospital battle casualty deaths to the total hospital battle casualty admissions during the survey period.
1Does not include 39 DOA casualties.
The type of causative agent as related to the principal wound is listed in table 130. Small arms accounted for approximately 15.11 percent of the hospital deaths while high explosive shell fragments (exclusive of mine, boobytrap, and bomb) were identified in 59.38 percent of the cases.
Table 131 correlates the principal wound with the time of death and the hospital admission, anesthesia, and surgery.
1Cases of blast, crush, and mutilating injury could not be classified in this manner, and number is less than total of 1,450.
1Lived less than 1 hour.
CAUSES OF DEATH
Certain problems were encountered in the classification and arrangement of this material. The Adjutant General of the Fifth U.S. Army and The Adjutant General of the U.S. Army report battle casualty deaths as "killed in action" or "died of wounds" (the latter includes those dying of injuries incurred in action). Hospitals report deaths according to a classification of principal wounds. Generally speaking, all battle casualties who die are said to die of wounds or injuries incurred in action. All of the cases reported in this study may be said to have died either of wounds or of injuries incurred in action against the enemy. Table 132 classifies the cases as to region of primary trauma leading to death. This classification is comparable to those just mentioned. For the purposes of this study, however, such classifications have been deemed inadequate.
A battle casualty who suffers a laceration of the popliteal artery may or may not lose sufficient blood to lead to severe shock, and death. If he does, the primary cause of death according to conventional reports is a wound of
1Generalized conditions involving more than one region.
the posterior aspect of the knee, with laceration of the popliteal artery. For the purposes of this report, the important desideratum in such a case is that the immediate or precipitating cause of death is shock (peripheral vascular failure).
While fully aware of the controversial nature of the subject, the decision was made to include the uncorrected state of shock as an immediate or precipitating cause of death, along with other more specific, standard diagnoses. It may be contended, of course, that such patients actually die of their wounds and the severity of the trauma attending them and that the shock which is present is a syndrome reflecting a profound pathologic alteration of normal hemodynamics and is not an acceptable diagnosis. However, in this study, as just stated, each case has been classified as to primary trauma leading to death (the conventional primary or basic diagnosis), and the liberty of employing the concept of the state of shock as a "diagnosis" for the immediate or precipitating cause of death (the conventional secondary diagnosis) allows for a more complete classification of the causes of death for comparison and study. This sets in relief that important group of cases which succumbed from the gravity of their wounds in a state of uncontrolled shock. It seems that this group of cases is worthy of the special attention afforded by such a classification.
Shock was selected as the immediate cause of death in 523 cases in this series. A special study was made on this group and is presented on page 511. The criteria used in naming shock as an immediate cause of death are discussed there and are apparent in the information tabulated.
"Neural trauma and/or intracranial hemorrhage or clot" was listed as the immediate cause of death in 212 cases and is second on the list of the immediate causes of death, as is shown in tables 133 and 134 and in the tabulation which is to follow. The relative importance as a lethal factor of the brain damage produced by the missile and the damage produced by an expanding intracranial hematoma was often difficult to determine. It seemed unwise, considering the available information and the qualifications necessary for evaluation, to attempt to separate these cases into two groups. It may be mentioned here that only 15 cases in whom the principal wound was intracranial were listed as dying of shock, while 210 were listed as dying of neural trauma or clot. (All 235 cases in these two categories were listed also under the heading "Primary trauma leading to death, intracranial.") Nephropathies were third on the list, and their incidence was relatively constant except during the first 3 months of the period covered by this report. The low incidence at that time may be attributed to failure of recognition and is therefore apparent rather than real.
1See tabulation on text page 487 for the total list of the immediate causes of death in the 1,450 cases.
In the first survey period, clostridial myositis was the third leading cause of death, the 35 cases comprising 6.5 percent of all deaths, and 0.28 percent of hospital battle casualty admissions. In the last period, it fell to the bottom of the list, with only one death attributed to it, comprising 0.6 percent of the deaths studied, and only 0.01 percent of all battle casualties admitted to hospitals. The educational program concerning clostridial myositis and the study of the problem conducted by Maj. Floyd H. Jergesen, MC, and Lt. Col. F. A. Simeone, MC, coupled with the more complete surgery on all wounds, the more liberal use of blood, and the advent of the extensive use of penicillin were important factors in effecting this striking reduction in mortality and the corresponding reduction in the incidence.
Peritonitis tended to show a slight increase in its percentage of the total battle casualty admissions and a more pronounced increase in its percentage of the deaths studied. There are two factors which may have contributed. First is the reduction in mortality from shock, clostridial myositis, extremity wounds,
1Corrected to allow for the percentage of hospital battle casualty deaths not studied in each period.
and unclassified wounds in the course of the 17 months covered by the study. This has led to a relative increase in peritonitis deaths, deaths from intracranial wounds, and other wounds or complications, the incidence of which was more or less inevitable. The second factor is the increase in the percentage of autopsies performed which probably accounts for the apparent but slight increase in the number of peritonitis deaths as compared to hospital battle casualty admissions.
The only striking variation in mortality from pneumonia is in the April-July 1944 period, in which pneumonia deaths comprised only 1.2 percent of the deaths studied as compared to the average of 3.4 percent for all four periods. It is the only one of the four periods which did not include winter months.
Tables 135, 136, and 137 compare the region of principal wound, the immediate cause of death, and the region of primary trauma. Attention is directed to the incidence of fat embolism. This diagnosis was not recorded except when microscopic reports indicated large amounts of fat in the pulmonary sections and the record indicated a clinical behavior justifying the diagnosis. It may be noted (table 148) that the diagnosis of fat embolism was evident in 22 additional cases in which it was listed as a contributory condition rather than as the immediate cause of death.
Thrombotic embolism and tracheobronchial obstruction from aspirated vomitus, blood, or mucus appear quite prominently in the leading causes of death. Their relative incidence showed a definite increase and the actual incidence perhaps a slight increase in spite of recognition of their importance and the inauguration of prophylactic measures early in the campaign.
1Involving more than one region, a miscellaneous group, excluding shock.
1Record inadequate in description of wounds.
Tables 138 through 149 deal with the total reported incidence of immediate and contributing causes of death. In this report, they are the best source of information regarding the incidence of any one condition. All the figures in the column under "Immediate cause of death" represent evident or confirmed incidence. The figures in the middle column represent both evident and suspected evidence, but in every instance they are separated and properly identified by the index column. The same applies to the total figures in the last column.
1Probably somewhat lower than the actual incidence.
The figures are believed to be lower than the actual incidence inasmuch as they represent only the reported incidence, and inasmuch as the records at times are not complete. The incidence figures on shock are perhaps nearer the actual than most of the other figures, because many indications of the presence of shock may be found in the record when it is present.
1Probably somewhat lower than the actual
1Probably somewhat lower than actual incidence.
1Probably somewhat lower than the actual incidence.
1Probably somewhat lower than the actual incidence.
1Probably somewhat lower than the actual incidence.
1Probably somewhat lower than the actual incidence.
1Probably somewhat lower than the actual incidence.
1Probably somewhat lower than the actual
1Probably somewhat lower than the actual incidence.
1Probably somewhat lower than the actual incidence.
1Probably somewhat lower than the actual incidence.
In this section, the cases in each of the principal wound groups are considered separately, and in each of the subdivisions a tabulation lists the immediate cause of death for the cases in that particular group.
1. The immediate cause of death in the 297 cases in which the principal wound was intracranial is as follows:
4Additional detailed information on surgery, anesthesia, replacement therapy, chemotherapy, oxygen therapy, and other miscellaneous data are presented in appendix F, p. 813.
2. The immediate cause of death in the 27 cases in which the principal wound was intravertebral is as follows:
3. The immediate cause of death in the eight cases in which the principal wound was maxillofacial is as follows:
4. The immediate cause of death in the 25 cases in which the principal wound was cervical is as follows:
1Includes 5 cases of cardiorespiratory embarrassment plus trauma and hemorrhage and 6 cases of trauma and hemorrhage.
5. The immediate cause of death in the 138 cases in which the principal wound was intrathoracic is as follows:
1Includes 66 cases of cardiorespiratory embarrassment plus trauma and hemorrhage, 2 cases of contamination or sepsis plus trauma and hemorrhage, and 2 cases of trauma and hemorrhage.
6. The immediate cause of death in the 212 cases in which the principal wound was thoracoabdominal is as follows:
7. The immediate cause of death in the 59 cases in which the principal wound was combined intra-abdominal and intrathoracic is as follows:
8. The immediate cause of death in the 408 cases in which the principal wound was intra-abdominal is as follows:
9. The immediate cause of death in the three cases in which the principal wound was of the abdominal wall is as follows:
10. The immediate cause of death in the four cases in which the principal wound was upper extremity, soft tissue only, is as follows:
11. The immediate cause of death in the 10 cases in which the principal wound was upper extremity, bone and soft tissue, is as follows:
12. The immediate cause of death in the 31 cases in which the principal wound was lower extremity, soft tissue only, is as follows:
13. The immediate cause of death in the 114 cases in which the principal wound was unclassified multiple is as follows:
SPECIAL STUDIES ON INTRA-ABDOMINAL WOUNDS
In 408 cases (28.1 percent) of the 1,450 deaths studied, the principal wound was intra-abdominal. Adding the 212 cases having thoracoabdominal wounds and the 59 cases having combined intra-abdominal and intrathoracic wounds, a total of 679 (46.8 percent) deaths were due to wounds of the abdomen. The latter two groups are not included in the study in this section.
The group of 408 cases in which the principal wound was intra-abdominal have been studied as a group in the preceding sections of this chapter (p. 501). In this section, the 408 cases are considered in further detail.
Shock was the immediate cause of death in 43.6 percent of those 408 deaths in which the principal wound was intra-abdominal. An analysis of this group of shock deaths in abdominal wounds (178 cases) is presented in tables 150 through 153 and the tabulations which follow. It was found that 30.9 percent died before surgery in this group as compared to 7 percent in the remaining cases (table 154). Contamination from a perforated hollow viscus was a factor in 65 percent of those dying from shock (table 151) which was less than the incidence of 74 percent in the rest of the group. Hemoperitoneum or continuing hemorrhage was noted in 64 percent of the shock group and in 70 percent of the remainder. There was very little difference in the incidence of peritonitis in the two groups, the figure approximating 21 percent. Likewise, there was little difference in the incidence of associated wounds in the two groups (table 152).
In the study of the time interval between wounding to death in the cases with intra-abdominal wounds and dying of shock, it was found that 11 cases lived less than 1 hour and 35 cases died before induction of an anesthesia with an average survival time of 16 hours.
1Excludes the DOA and the dying on admission.
The following is a breakdown of the 178 cases in which the principal wound was intra-abdominal and the immediate cause of death was shock:
1Contamination or sepsis was a factor in 116 cases
and not a factor in the remaining 62 cases.
In the 178 cases in which the principal wound was intra-abdominal and the immediate cause of death was shock, there was an incidence of 193 associated and, in many instances, multiple wounds, as follows:
There were no associated wounds in 60 of these 178 cases.
The records of plasma and blood administered can be very difficult to interpret. In a surprisingly large percentage of cases, there was no record of any blood transfusion. It is possible that some received blood and no record was made, but also probable that in the majority no blood was administered. The averages given (table 152) are based only on those cases in which blood was given and a record made of its administration. The data on the amount of plasma administered before admission represent the replacement therapy carried out in battalion aid stations (fig. 263), collecting stations, and clearing stations. While it is believed that only the minimum amount of plasma necessary to insure transportability of the patient should be given, just what that amount is in each case has to be determined by the individual medical officer in charge. That his judgment had been excellent in nearly every case is a statement to which medical officers in Army hospitals will attest. Comparing the averages and the number receiving blood in the group dying in shock with the whole group of cases, it was found that a larger percentage of cases received a larger average amount of blood in the shock group than in the group as a whole. Inasmuch as this series involved only deaths and there were no figures at hand for the cases with intra-abdominal wounds who lived, comparisons could not be made with a group of cases in which therapy was adequate.5
The percent of bullet wounds in the shock deaths in the intra-abdominal group was 17.4 percent (table 153) as compared with 19.6 percent in the entire intra-abdominal group, while in the whole series (1,450) it was only 15.0 percent.
1The type of wound in this group was penetrating in 125 cases and perforating in 53 cases.
The following tabulation lists the miscellaneous conditions occurring in the group of 178 cases with intra-abdominal wounds who died of shock:
Myocardial decompensation was evident in only two cases, and, in these, excessive administration of plasma and blood was thought responsible. Pulmonary edema was noted in 13 cases in the group. As this is an unusual occurrence in uncomplicated shock, a search was made for factors predisposing to pulmonary edema. All 13 cases received plasma and blood before surgery. The average units received were little different from the averages for those receiving plasma and blood in the rest of the group in which, however, a substantial number received none. It was difficult to draw any conclusions regarding the role plasma and blood played in the appearance of pulmonary edema in this group. Thoracic trauma, blast trauma, and pneumonia probably contributed to the incidence of "pulmonary edema."
Study of blood pressure records revealed that 17 of the 55 recorded admission blood pressures were zero. The lowest pressure recorded was zero in 34 of the 70 cases where records were available. The average duration of surgery in this shock group approached 2˝ hours. All cases coming to surgery received ether anesthesia. Thiopental sodium (Pentothal sodium) was used once and nitrous oxide 40 times for induction.
Table 154 and the tabulations which are to follow deal with those cases (230) in which the principal wound was intra-abdominal but the immediate cause of death was not shock. It should be noted that there was no evidence of shock in only six of these cases. The remainder had evidence of shock at some time during the course of their hospital stay.6 Analysis of shock as a contributory or associated condition is included in the study of this group of cases.
The incidence of shock as a contributory or associated condition in the group of 230 cases in which the principal wound was intra-abdominal and the immediate cause of death was not shock follows:
Miscellaneous findings in 230 cases in which the principal wound was intra-abdominal but the immediate cause of death was not shock but with shock as a contributory or associated condition (224 cases) were as follows:
In the 230 cases in which the principal wound was intra-abdominal but the immediate cause of death was not shock, the incidence of associated wounds was as follows:
There were no associated wounds in 70 of the 230 cases.
A further breakdown of the group of 408 cases in which the principal wound was intra-abdominal is presented in tables 155 through 159. The data presented in those tables are for a group of 175 cases in which peritonitis was
evident or suspected to be present. It was believed that a better picture of intra-abdominal wounds might be obtained if they were not complicated by factors originating from concomitant wounds of the chest and diaphragm. Those with peritonitis and suspected peritonitis were examined in three groups (table 155). The first group was composed of those in which peritonitis was the immediate cause of death. In the second group, peritonitis was evident but not the immediate cause of death. This included the cases listed under contributory or associated conditions as "peritonitis, severe" and "peritonitis, mild or moderate." The third group was made up of those cases in which peritonitis was suspected but the evidence was not sufficient to confirm its presence.
CASES IN WHICH THE IMMEDIATE CAUSE OF DEATH WAS SHOCK
The 523 cases which have been listed under this heading were those in which there was good evidence of peripheral circulatory failure initiated by the initial trauma and hemorrhage and perpetuated by trauma and hemorrhage with or without the added shock-producing factors of cardiorespiratory embarrassment, peritoneal contamination from a wound of a hollow viscus or early sepsis, or any combination of these factors. The data on the "Etiology of shock" reveal the evidence of these various factors. No effort was made to separate the factors of trauma and hemorrhage, as both occurred in varying degrees and proportions in every battle casualty. In 13 cases, recurrent or delayed abdominal hemorrhage was a factor. In the 245 cases who died of shock after primary surgery, only 43 lived more than 24 hours after the surgery.
Tables 160 through 165 which follow relate to the 523 cases in the series of 1,450 deaths in which shock was listed as the immediate cause of death. In addition, there were 750 other cases in which shock was a contributory or associated condition. There was no evidence of shock in only 177 of the 1,450 deaths studied. It is not within the province of this report to discuss in detail the etiology of shock. However, it should be stated that clinical experience and laboratory investigations demonstrated that loss of whole blood was the most important factor in the vast majority of battle casualties in shock. The amount of blood lost was far in excess of previous estimates. In 1945, whole blood was given to 40.6 percent of the battle casualties admitted to Fifth U.S. Army hospitals at a rate of 2.52 pints per casualty transfused.7 Many casualties were given as much as 6 or 8 pints of blood and a few even more in the first 24 hours after their admission to the hospital. Plasma loss per se was found only in burns, crush injuries, gas gangrene, sepsis, and gross
contamination of the peritoneal or pleural cavities.8 In the latter two categories, plasma loss was often less than whole blood loss. Inasmuch as blood was not available except in exceptional circumstances at battalion aid and collecting and clearing stations, some of the most severely wounded casualties, or those in the most severe grade of shock from their wounds, were often given large quantities of plasma to render them transportable to the hospital. These casualties were frequently again in severe shock by the time they arrived at the hospital, and further resuscitation was complicated because the remaining blood in their vascular tree was well diluted with plasma.
Among contributing factors in shock deaths were the following:
1. The use of large quantities of plasma to combat lowered blood volume when the loss has been of whole blood.
2. Unrecognized and/or uncontrolled continued bleeding.
3. Inadequate or poorly timed blood replacement with whole blood.
4. Delayed surgery in those cases in which there has been gross contamination of peritoneal and pleural cavities with contents of the gastrointestinal tract, or in which sepsis is developing.
5. Failure to recognize and/or control factors leading to cardiorespiratory embarrassment. Included in this group are hemothorax, pneumothorax, cardiac tamponade, tracheobronchial obstruction from blood or mucus, painful chest wall wounds, and gastric dilatation.
6. Failure to control pain by morphine, procaine hydrochloride (Novocain) nerve block, proper splinting of painful extremity wounds, and timely surgery.
1Excludes the DOA and those dying on admission.
NOTE.-Key for roman numerals:
1Excluding the gradual terminal
decline immediately preceding death.
NOTE.-Key for roman numerals:
NOTE-Key for roman numerals:
PIGMENT NEPHROPATHY IN BATTLE CASUALTIES
The development of progressive oliguria and anuria in battle casualties resuscitated from shock and apparently on the road to recovery following extensive surgical procedures led to the death of a significant number of severely wounded soldiers. Death usually occurred between the fourth and eighth days after the wound was incurred. At autopsy, the kidneys were observed to be somewhat enlarged, and on microscopic examination pigment casts were seen in the distal convoluted and collecting tubules. The proximal tubules were dilated, and a varying degree of necrosis of the distal tubules was observed, with some inflammatory reaction in the adjacent stroma. The capillary tufts in the glomeruli showed no changes, but there was in some cases slight swelling of the cells in Bowman's capsule. This lesion has been variously termed pigment nephropathy, hemoglobinuric nephrosis, and lower nephron nephrosis.
Among the 1,411 deaths, lower nephron nephrosis or pigment nephropathy led to death in 68 cases (table 166) and contributed to death in 31 others. It was suspected to have been present in 57 additional cases. Autopsy was performed in all but 9 of the 99 cases in which pigment nephropathy was known to be present, and microscopic study of renal sections was reported in 67 of the 90 cases in which autopsy was performed.
A study of the 99 cases in which pigment nephropathy was known to be present forms the basis of this presentation. Of significance are the severity and multiplicity of wounds encountered in this group. The following tabulations list the site of the principal wounds and of the associated wounds in this group of 99 cases of pigment nephropathy:
It will be noted that the abdominal cavity was involved in 59 cases and that intra-abdominal wounds were present as associated wounds in 2 more cases and suspected in 3 others. In only 20 cases were no wounds present other than the one or ones listed as principal wounds. The 149 associated wounds occurred in 79 cases, for a total of 238 wounds.9
In all the deaths in battle casualties studied, attempt was made to ascertain an immediate cause of death. Lower nephron nephrosis was regarded as the immediate cause of death in 68 cases. In 31 cases, some other cause was thought to be the immediate cause of death, as is shown in the following tabulation:
The so-called immediate cause of death, however, fails to give a complete picture of the multiplicity of pathologic conditions existing in this group of 99 cases. The contributory or associated conditions existing in this group are shown in the tabulation which follows:
Pulmonary complications were so frequent as to be almost the rule. In many cases, the giving of intravenous fluids in the absence of urinary excretion led to high volume of the blood, cardiac failure, and pulmonary edema. Toxic hepatic degeneration was present in 16 cases, epidemic hepatitis in 4 cases (suspected in 1 more), and septic hepatitis secondary to trauma in 2 cases (suspected in 3 more). There was recorded evidence of renal trauma in 18 of the 99 cases, and a ureter had been traumatized or tied in 3 other cases. Fat embolism was the immediate cause of death in 3 cases, contributing cause of death in 8 cases, and was suspected as contributory to death in 4 more cases. The 11 cases in 99 represent an incidence of 11 percent, which is considerably higher than in the whole series of 1,411 battle casualty deaths, in which 49 cases constitute only 3.5 percent. It is also interesting to note that, in the 49 patients known to have pulmonary fat embolism, 11 had pigment nephropathy. Severe reactions from blood transfusion were noted in only 3 of the 99 cases. Gross infection was evident in 61 cases.
One outstanding feature in the cases in which anuria developed was the severity of the shock which occurred sometime between wounding and the development of renal insufficiency. In the 99 cases in which pigment nephropathy was known to exist, the lowest recorded blood pressures, along with other data relative to shock, are as follows:
The five cases, the records of which gave no evidence of shock, are of sufficient interest to warrant presentation of case summaries (cases 3, 4, 5, 6, and 7).
It must be remembered that many of the records were rather incomplete. Data regarding the duration of low blood pressure were available in only a few instances. No data concerning the level of blood pressure before admission to a hospital are available. The amount of plasma administered before admission is perhaps the best index of shock at that time. The number of
units of 250 cc. of plasma administered in 99 cases of pigment nephropathy before admission to a hospital installation was as follows:
There was evidence of shock in 94 of the 99 cases of pigment nephropathy. Trauma and hemorrhage were the leading causative factors in the development of shock. Additional contributory factors were cardiorespiratory embarrassment and contamination of the peritoneum or of an extremity. The amounts of plasma and blood used after admission to the hospital are further indexes of the degree of shock in these patients. The recorded data available concerning the administration of plasma and of blood are shown in the following tabulation:
Treatment with oxygen might be expected in a larger percentage of patients than is shown in the following tabulation:
The operating time for primary surgical treatment, shown in the tabulation which follows, is a further index of the severity of the wounds in this group of cases.
Unfortunately, the time was not stated in 62 of the cases; no operation was performed in 11 cases. In the remaining 26 cases, however, it was seen that in only one case did the operation last less than 1˝ hours, while in the largest group of cases the operating time was from 3 to 3˝ hours.
Data concerning anesthesia in the 68 patients who died of pigment nephropathy are presented in table 167. It will be noted that, with the exception of four patients who died before anesthesia was complete, all of whom had crush injuries, all had been given ether. In table 168, the anesthesia in 31 cases in which pigment nephropathy was a contributing cause of death is recorded. Of this group, seven patients died before anesthesia was complete; one had local anesthesia only; and all of the rest had ether anesthesia in one form or another. The patient who had local anesthesia only had an intracranial wound and died of pneumonia, septic hepatitis, and jaundice. There was a record of adequate urinary output and no evidence of shock. On the basis of microscopic autopsy alone, the diagnosis of pigment nephropathy was made. Data for seven patients who died before the induction of anesthesia
in this group are presented in table 169. The diagnosis of pigment nephropathy in each of these cases is based on microscopic study of renal sections. All the patients had severe wounds; most of them died after a comparatively short time of being wounded, and correction of shock was doubtful or shock was completely uncorrected in all but one patient. Data concerning the amount of urine passed were unavailable. Since ether was considered to be the anesthetic of choice in all battle casualties with shock or severe wounds, no significance can be attached to the high incidence of ether anesthesia in this group of patients with pigment nephropathy.
1All were known to have had ether, alone or in
combination with another agent.
1Specific agent not known.
1Diagnosis of pigment nephropathy in each instance was based on microscopic study of renal sections.
When the first cases of anuria were encountered, the sulfonamide drugs were regarded as the probable causative factor. Sulfanilamide powder was dusted into almost every wound on the battlefield, and most of the wounded soldiers had taken 4 gm. by mouth before reaching the hospital. Early in the period under study, it was common practice to administer 5 gm. of a sulfonamide drug intravenously to all with abdominal wounds immediately on admission to the hospital and to repeat this dose at intervals of 12 to 24 hours thereafter. With the appearance of anuria, this practice was discontinued, and no sulfonamide drug was given intravenously until 12 hours after operation and only after the patient had fully reacted from shock. At the same time, the amount of sulfanilamide dusted into the peritoneal cavity was limited to 5 gm. and the amount in all wounds to 10 gm. That sulfonamide drugs were
a causative factor at least in one case, cannot be refuted. That they were not the only factor except in a few cases, likewise, was evident from subsequent studies. In 30 of the 68 cases in which pigment nephropathy was the direct cause of death and in 14 of the 31 cases in which pigment nephropathy contributed to death, there was no record of sulfonamide therapy, excluding the sulfanilamide powder dusted into wounds at the time of the first aid dressing.
The microscopic observation of a lesion termed hemoglobinuric nephropathy focused attention on blood transfusion as a causative factor. Before the establishment of a blood bank unit in the Mediterranean theater, reactions from mismatched and unmatched transfusions did occur in a few instances. However, anuria continued to develop after the use of group O blood from the blood bank. Then it was thought that the transfusion of a large quantity of group O blood to group A or group B recipients might be responsible for anuria in some of the cases; however, low titer group O blood (containing anti-A and anti-B iso agglutinins in a titer of less than 1 to 120) was used for all except group O recipients, and it was later ascertained10 that the incidence of pigment nephropathy in the persons of the four blood groups paralleled the relative incidence for persons of the four groups in the general population. In a separate article,11 a case of Maj. James M. Mason's was mentioned in which a group A recipient received 5,500 cc. of low titer group O blood before and during operation for a thoracoabdominal wound, which involved the removal of one kidney. There was no evidence of insufficiency in the remaining kidney, and the patient made an uneventful recovery. It was likewise demonstrated12 that the shock occurring in battle casualties was due in most instances to loss of whole blood and that the apparently massive doses of blood used in resuscitation of these patients were excessive in only a few instances. In most cases, determinations of the volume of blood established the fact that not enough whole blood was being used in the resuscitation of these patients. It was also observed that many patients showing gross hemoglobinuria did not always experience renal insufficiency, while, on the other hand, in many of the fatal cases of pigment nephropathy hemoglobinuria was never apparent grossly.
Early in 1944, at the same time that a reduction in the use of sulfonamide drugs was effected, the use of sodium bicarbonate to render the urine alkaline was encouraged. In many cases, it was given by mouth as soon as treatment with sulfonamide drugs was started; in others, it was given intravenously before sulfonamide medication and blood transfusion. Records regarding this treatment were seldom complete, but in the 99 cases of nephropathy the use of sodium bicarbonate was reported in 21 cases.
The hepatorenal syndrome was considered as a mechanism which might account for anuria in some of the cases. The reports of Orr, Helwig, and Schutz13 constituted the chief source of information for American surgeons concerning renal shutdown associated with trauma. It was apparent, however, that the majority of patients seen did not present evidence of hepatic damage, although such damage was present in no inconsiderable percentage. Review of the microscopic renal observations in the cases reported by Orr and Helwig would lead one to believe that the condition they described was pigment nephropathy.
Lucké14 reviewed 538 cases in which the disease was fatal, the records and material of which were received at the Army Institute of Pathology during the war. He found the characteristic renal lesion in 11 groups, which included cases in which there were battle wounds, crushing injuries, abdominal operations, burns, reactions from blood transfusion, intoxication due to sulfonamide drugs, heat prostration, malaria due to infection with Plasmodium falciparum (black-water fever), poisoning due to a variety of agents, hemolytic anemia, edema, and such unrelated conditions as uteroplacental damage, acute pancreatitis, and rickettsial disease.
With increasing experience with the condition, it became the opinion of many that the severe degree of shock occurring in most of the cases must be responsible at least in part for the development of nephrosis. In the fall of 1944, a board15 for the study of the severely wounded was appointed by Col. Edward D. Churchill, MC, Consultant in Surgery, Mediterranean theater. This board made elaborate studies, both clinical and laboratory, on battle casualties in severe shock16 when admitted to forward hospital installations and all observations of practical value were made available immediately in the forward hospitals. Before this time, clinical observation by many and laboratory investigation by Stewart, Lalich, and others had led to the general belief that shock in persons suffering injury in battle was in most cases due to loss of whole blood. The studies of the board confirmed this opinion and defined the exceptions to the rule. It was learned that in the cases in which nephropathy developed the observation of a benzidine-reacting pigment in the specimens of urine was a constant feature. Study of this pigment by a chemical method showed that it was myoglobin in cases of crush injury but that in the other cases it might be hemoglobin or myoglobin or a combination thereof. Except in the cases in which there were crush injuries, it was impossible to predict from the nature of the injury what type of pigment would be seen in the urine. Mallory, a member of the board, observed that it was not possible by micro-
scopic study of the kidneys to determine whether a lesion had been produced by poisoning due to sulfonamide drugs, mismatched transfused blood, or other factors. Mallory pointed out that the deposit of pigment in the distal convoluted and collecting tubules does not seem to be the first pathologic change in the kidneys. In 11 of their patients who died of injury within 72 hours, only 2 showed pigment casts in significant numbers.
Before the appearance of pigment casts, a fine fat vacuolization of ascending limbs of Henle's loops appears. Mallory stated that this appears in 75 or 80 percent of patients who experienced shock, regardless of whether clinical evidence of renal insufficiency develops or not, and that the process is reversible. He expressed the belief that the pigment casts play no role in the initiation of renal insufficiency following shock but that one cannot state that they have no effect in the later stages of the disease. The dilatation of the renal tubules proximal to the casts and about them would lead to the assumption that they do produce a degree of obstruction, at least in the involved tubules.
Case 1.-An infantryman suffered a perforating wound of the left lower part of the abdomen and the left hip from a machinegun bullet. He was admitted to the battalion aid station 10˝ hours later; 6˝ hours more elapsed before his admission to a field hospital. At this time, the blood pressure was unmeasurable, He was given 500 cc. of plasma and 2,500 cc. of low titer group O blood prior to operation. A catheterized specimen of urine appeared blood stained. A laparotomy was performed 7 hours after admission and 24 hours after the wound had been incurred, and a laceration of the jejunum and early severe peritonitis were observed. The laceration was sutured; the peritoneum was irrigated with isotonic solution of sodium chloride and 100,000 units of penicillin; and 10 gm. of sulfanilamide were deposited in the peritoneal cavity. The wound at the left hip, which had produced a compound fracture of the greater trochanter, was debrided. He was then given 5 gm. of sodium sulfadiazine intravenously. Treatment with penicillin, 25,000 units every 3 hours, was started on admission. The blood pressure at the end of operation was unmeasurable, but within 2 hours it rose to 100 systolic and 80 diastolic. His postoperative course was characterized by progressive oliguria, edema, uremia, disorientation, and respiratory distress. Death occurred on the eighth postoperative day. On the first postoperative day, he received 500 cc. of blood, 500 cc. of plasma, 1,000 cc. of dextrose in isotonic solution of sodium chloride, and 5 gm. of sulfadiazine. On the second postoperative day, he was given 500 cc. of blood, 2 units of plasma, 2,000 cc. of dextrose in isotonic solution of sodium chloride, and 5 gm. of sulfadiazine. No more sulfadiazine was given and no more blood except 1 pint (about 473 cc.) the day before death. Two days before death, the nonprotein nitrogen in the blood was 91 mg., chlorides 605 mg., and sulfadiazine 13.23 mg. per hundred cubic centimeters. His urinary output on the day of operation was 150 cc., and on successive days it was 200 cc., 350 cc., 300 cc., 600 cc., 400 cc., undetermined, and 75 cc.
At autopsy, the peritoneal cavity contained a small amount of thick grayish yellow foul-smelling pus, and the viscera were plastered to one another and to the parietes by a coating of exudate up to 4 mm. in thickness. The liver was approximately 50 percent heavier than normal, and the capsule was tense beneath the sheet of exudate on its surface. On sectioning, the cut surface was nutmeg brown, with well-defined architectural units. The spleen was doubled in size, and the capsule beneath the exudate was grayish red. The kidneys were moderately enlarged; the capsules stripped readily, revealing surfaces which were darker brown than normal, with fine dark red points and lines scattered throughout.
The cortices were slightly widened; the pyramids were swollen and discolored by brown and red lines paralleling the tubules. The apexes of the pyramids were dark brownish yellow. The lungs did not collapse normally, and their weight was decidedly increased, particularly on the right side. Cut surfaces were moist and released blood-stained mucoid fluid on pressure. There were slightly firm purplish red areas scattered throughout all the lobes, but these were confluent only in the lower parts of the right upper and right lower lobes. Examination of the renal sections showed that the glomeruli were moderately congested; the tubules were slightly dilated. The distal convoluted and collecting tubules contained numerous brown granular and hyaline casts. Many tubules contained desquamated epithelial cells and polymorphonuclear cells. One tubule showed a decided proliferative reaction interspersed with polymorphonuclear cells. Here the inflammatory process extended into the interstitium. There were scattered crystals of a sulfonamide drug within the lumens of the distal tubules. The interstitial tissues contained engorged blood vessels, and there was extravasation of small red cells. Microscopic pathologic diagnoses included pigment nephrosis, hemorrhagic bronchopneumonia, acute purulent perihepatitis, and perisplenitis.
Case 2.-A 21-year-old soldier was injured during a bombing raid when a stone building collapsed on him. He was extricated from beneath a pile of stone after 32/3 hours and reached an evacuation hospital 15 minutes thereafter. There was no visible evidence of traumatism, and skeletal roentgenograms revealed nothing of significance. His blood pressure was 104 systolic and 74 diastolic, and the pulse rate was 120. The urine was wine colored, with no red cells. Approximately 7 hours after admission, he was given 500 cc. of type O blood and then 1,000 cc. of 5 percent dextrose. Four or five hours later, he went into a state of shock. This was evident by pallor, loss of radial pulse, and no blood pressure. A transfusion was started, but when the hematocrit was observed to be 70 percent it was discontinued, after 300 cc. were given, and dextrose with isotonic solution of sodium chloride substituted. The blood pressure rose to 100 systolic and 80 diastolic. A specimen of urine was chocolate colored. He complained of many points of muscular soreness and tenderness, and the areas were tense and brawny on palpation.
During the succeeding 9 days, he remained oliguric, the daily output of urine ranging from 50 to 100 cc., with an intake of about 3,000 cc. of fluid. Sodium bicarbonate was given daily in 2.5 percent of solution. The patchy muscular induration increased. The urine became normal in color on the third day but still had a positive benzidine reaction. On the sixth day, the face was puffy, and there was pitting edema over the sacrum. The blood pressure was 150 systolic and 110 diastolic. Magnesium sulfate was given intramuscularly. During the next 3 days, the edema increased and the hypertension persisted; epistaxis became frequent; and death occurred with relative suddenness a little less than 10 days after the injury. The level of nonprotein nitrogen in the blood reached a total of 291 mg. and creatinine 12.2 mg. per hundred cubic centimeters the day before death occurred. A check for myoglobin on one specimen of urine early showed a concentration of 588 mg. per hundred cubic centimeters. At autopsy, all muscles appeared paler than normal and scattered throughout the skeletal musculature were many focal areas of traumatic damage. In most instances, these were segments of muscles closely proximate to bone. Larger foci noted were in the flexor group of the left forearm, the left vastus medialis, the lower quarter of the right sartorius, and all of the right soleus. The general pattern was a pigmented grayish white area in the muscles surrounded by a hemorrhagic border. Some of these areas appeared translucent and like fish flesh; others were frankly necrotic, with an opaque slighty grayish infiltration. Some foci appeared almost chalky, and the muscle fibers in the involved areas were friable and easily torn. The kidneys weighed 550 gm. They were symmetrically enlarged, and the vessels of the perirenal fat were engorged. One focus of hemorrhage in this fat was noted at the lower pole of the right kidney. It was entirely extracapsular. The capsules stripped readily and left pale smooth surfaces. The arteries and veins were patent. On sectioning, the cortex was pale and swollen. The surfaces appeared moist;
the pyramids were dark, with a hint of brown in predominant redness. The vessels were not engorged, and no gray zone was present at the corticomedullary junction.17
Case 3.-A soldier was wounded in action near Cassino, Italy, by artillery shell burst. He was admitted to an evacuation hospital approximately 4Ľ hours later, in good condition and showing no signs of significant loss of blood. In the shock tent, he was given 60 grains (3.9 gm.) of sulfadiazine and 500 cc. of plasma. Thirty minutes later, in the operating tent, the wound of entrance overlying the head of the left femur posteriorly was debrided, and the track followed up toward the anterior-superior iliac spine, where a counterincision was made. A foreign body was removed without difficulty, along with two or three comminuted bone fragments. A penetrating wound of the left forearm was then debrided and the foreign body removed. Both wounds were treated with sulfanilamide powder and petrolatum-impregnated gauze. During the operation with the patient under gas, oxygen, and ether anesthesia, a blood transfusion was started. Later, while the patient was still on the operating table and still under anesthesia, generalized shaking chill, or rigor, began. The transfusion was discontinued and 500 cc. of plasma given. The same blood was matched again and observed to be compatible, and the rest of it was administered without untoward reaction. Following the operative procedure, a catheter was inserted, and 120 cc. of dark blood-stained urine was obtained. From this time on, a catheter was employed every 12 hours. The bladder was still empty after 24 hours. His general condition remained essentially unchanged until approximately 8 hours before death, when he became irrational, breathing became irregular, and increasing pulmonary edema developed. He died approximately 72 hours following operation.
He had received no blood other than that previously noted. In addition to the aforementioned amount of sulfadiazine, he was given 8 gm. by mouth the first 24 hours but none thereafter. Post mortem, the gross examination of the kidneys, ureters, and the bladder failed to reveal any abnormality; however, microscopic examination of the kidneys revealed nephrosis of the lower nephron.
Case 4.-A crush syndrome developed in a soldier, similar to the one presented in Case 3, except that there was no history of low blood pressure at any time during the 4˝ days that he lived after injury.
Case 5.-A soldier suffered a perforating wound of the brain, a penetrating wound of the left jaw, and a perforating wound of the right shoulder. He was admitted to an evacuation hospital over 10 hours after the wound had been incurred. On admission, his blood pressure was 130 systolic and 74 diastolic; the pulse rate, 78; and respiration, 20. A roentgenogram of the skull showed that a foreign body 1.6 cm. in size had perforated the skull in the left parietal region, had passed through the parietal lobes, and had perforated the right frontal aspect of the skull, and had come to rest with the bone fragment before it under the scalp. A linear fracture, 12 cm. long, extended backward in the frontal bone on the left, from the depressed fracture entrance. The patient was comatose on admission. He exhibited palsy of the right seventh nerve and spasticity in all extremities. Debridement of the wound of the skull and the brain was performed about 6 hours after the patient's admission to the hospital. In addition, the wounds of the jaw and the shoulder were debrided. He was given 1,500 cc. of blood and 1,000 cc. of plasma during the operation. He remained comatose until his death. He had a relatively high temperature, with increased pulse rate and respiration. He received sodium sulfadiazine intravenously in a dosage calculated to produce a level in the blood of 20 mg. per hundred cubic centimeters. Oliguria developed about 5 days postoperatively, which progressed to complete anuria in 2 more days. Cystoscopy was performed, and the renal pelves were lavaged with sodium bicarbonate solution. Numerous sulfadiazine crystals were observed, particularly in the left renal pelvis. He died 7 days after he was wounded. Microscopic observations at
autopsy included indications of encephalomalacia, bronchopneumonia, and pigment nephrosis.
Case 6.-A soldier was wounded in action by a high explosive shell fragment 1 or 2 days before admission to an evacuation hospital. The exact date and the time of his wounding on Mount Porchia, Italy, were unknown. On admission, he was semistuporous and showed changes in his reflexes, and the roentgenogram showed depressed fracture of the right parietal bone, with a large bone defect and fragments of bone and metallic foreign bodies driven into the right cerebral hemisphere. The operative risk was considered poor, and the patient was given 500 cc. of plasma before operation, 500 cc. of blood during operation, and 500 cc. of blood shortly thereafter. Operation was performed under block anesthesia with procaine hydrochloride approximately 8 hours after his admission to the hospital. Partial craniectomy, with thorough debridement of the wound of the brain and dural repair, was accomplished. At termination of the operation, the patient was sent to the ward in satisfactory condition, with a blood pressure of 120 systolic and 70 diastolic, a pulse rate of 120, and a temperature of 100.2° F. Postoperatively, he received 10 gm. of sodium sulfadiazine intravenously, in two doses of 5 gm. each in the first 24 hours and 5 gm. intravenously in divided doses in the second 24 hours. Subsequently, he received sulfadiazine, 6 gm. daily by mouth, through the eighth postoperative day. He also received one unit of concentrated plasma twice daily for 8 days and four blood transfusions postoperatively. He was never entirely rational or lucid, but at times he responded moderately well to questions and talked coherently. Four days postoperatively, the patient had a crisis, characterized by clonic contractions of the right side of the body and face for a few seconds, followed by twitching for several minutes and a sudden rise of temperature to 107° F; the pulse rate was 160 and respirations, 52. All subsided quickly. His daily temperature, aside from this one episode, was from 102° to 103° F. On the ninth postoperative day, the patient was much weaker and drowsier and responded poorly to questions. He showed hemiplegia and facial paralysis on the left side, which had been present all along, plus weakness of several cranial nerves. Treatment with sulfadiazine was discontinued on this date, and his condition was considered critical. The next day he was much worse, presenting dyspnea, cyanosis, tachycardia, decided pulmonary congestion, jaundice, and coma. A diagnosis of terminal bronchopneumonia was made; the cause of the jaundice was not clear. At post mortem examination, it was noted that the common duct and larger branches were not obstructed and that the gallbladder was not enlarged. On sectioning, the hepatic tissue appeared to be deeply jaundiced, and the appearance was somewhat suggestive of a diffuse necrotic process. The parenchyma of both kidneys appeared to be within normal limits; the kidneys were about normal size, and the capsules stripped normally. The pelves of the kidneys were stained with bile, and the mucosa contained numerous pinpoint hemorrhages. No crystals were evident. There were no signs of infection in the wound of the brain. The diagnoses, based on gross pathologic studies, were nonobstructive jaundice, the cause of which was undetermined; bronchopneumonia; and hepatitis. The report of microscopic examination of the section of the liver was not available, but the following diagnoses, based on microscopic studies, were made: (1) Bronchopneumonia, (2) jaundice, and (3) slight hemoglobinuric nephropathy. The significance of the latter diagnosis is not entirely clear. This patient was carefully studied, and his daily urinary output was over 1,000 cc., except on the day of his death. It is perhaps incorrect to assume that hemoglobinuric nephropathy contributed to death in this case.
Case 7.-A soldier was admitted to a field hospital approximately 1 day after being wounded by enemy shellfire near Montecatini, Italy. He suffered compound fractures of the left tibia and fibula in the middle third, a compound fracture of the left clavicle, a compound fracture of the left scapula, and multiple penetrating wounds of the left buttock. All of his wounds were debrided under open drop ether anesthesia in the field hospital. Six days later, he was evacuated to an evacuation hospital, where he died 1 hour and 20 minutes after admission. There was nothing further in his record concerning his clinical course. Post mortem examination was done, and it was observed that both kidneys were enlarged, that
the cortex was pale and swollen and irregular in both kidneys, and that the capsule stripped easily. A diagnosis, based on gross pathologic studies, of nephrosis was made, the cause of which was unknown. There were no microscopic observations in this case. Also presented were bilateral pleural effusion, a hematoma in the upper lobe of the left lung, and pulmonary congestion and edema, as well as the wounds previously noted. While there was no evidence of shock recorded, it probably should be stated that the record was too inadequate to permit the conclusion that shock did not exist at one time or another.
The condition described as pigment nephropathy, or lower nephron nephrosis, occurs with a variety of conditions. In battle casualties, the renal damage is probably dependent on renal ischemia plus the excretion of pigment. The renal ischemia is vasoconstrictive in origin and occurs in patients in a state of shock and with related conditions. Whether or not the vasoconstriction is induced by a toxin elaborated from damaged tissues or by reflex vasomotor stimulation has not been definitely established. The pigment excreted may be myoglobin or hemoglobin. The source of the hemoglobin may be from transfused blood, intravascular hemolysis, and probably from other sources. The role of infection has not been clearly defined and should be made the subject of investigation. The influence of the various anesthetic agents should be studied.
Treatment should be prophylactic. Shock should be combated vigorously, with prompt restoration of the volume of blood to normal. This should be accomplished with the proper medium, which for most battle casualties is whole blood. Treatment with oxygen is of value in combating anoxia, which must result from vasoconstriction in the renal circulation. Injudicious use of sulfonamide drugs should be avoided, and discontinuance of their use in conditions predisposing to nephropathy should be considered. Dehydration should be avoided when possible and otherwise corrected as promptly as possible. Thorough surgical removal of all devitalized tissue and foreign bodies and provision of adequate drainage to infected areas is important.