History

CHAPTER VII

Study of Fifth U. S. Army Hospital Battle CasualtyDeaths¹

Howard E. Snyder, M.D., and James W. Culbertson, M.D.

From 1 January 1944 until the surrender of the German armiesin Italy on 2 May 1945 (the period covered in this study), 91,631 Americansoldiers serving in the Fifth U.S. Army were killed or wounded in action (table120). Of this total, 16,648 (18.2 percent) died on the battlefield or beforereaching a medical installation; 11,959 (13 percent) were treated and returnedto duty from the division area (fig. 258). Of the remaining 63,024 (68.8percent) 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) ofthese hospital battle casualty deaths were available for this study. Inaddition, the records of 39 casualties who were DOA (dead on arrival) at ahospital were utilized in many sections of this report. Gross post mortemfindings formed a part of 733 of these records (table 121). Microscopic autopsyreports were received on 349. Most of the clinical records were fairly complete,

TABLE 120.-Distribution of 91,631 FifthU.S. Army casualties in Italy, from 1 January 1944 to 2 May 1945, by category

Category	Number of casualties	Percent of casualties
Killed in action	16,648	18.2
Wounded in action:
Hospitalized, DOW (died of wounds)	1,631	1.8
Hospitalized, lived	61,393	67.0
Returned to duty without hospitalization	11,959	13.0
Total	91,631	100.0

¹The original three-volume report on which this chapter is based was submitted as a comprehensive survey and partial analysis of available information on 1,450 fatally wounded American soldiers. There has been a partial attempt to consolidate and interpret some of the findings, but there are still many lessons which may be drawn from this study.
Brig. Gen. (later Maj. Gen.) Joseph I. Martin, Surgeon, Fifth U.S. Army, at the time the study was started, encouraged and helped make possible the report. Col. Charles O. Bruce, MC, the Fifth U.S. Army surgeon during the latter months of the study, furnished needed advice. Maj. Richard A. Morrissey, SnC, statistician in the Fifth U.S. Army surgeon's office was a source of great encouragement.
To the cited personnel, as well as to the many individuals who have not been mentioned, we express sincere appreciation for their unselfish contributions.-H.E.S. and J.W.C.

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FIGURE 258.-Building occupied by fieldhospital platoon and four surgical teams, Porretta, Italy.

but, in some, much desirable information was missing.However, most of the autopsies were performed by the operating surgeons alreadyengaged in the arduous surgical tasks associated with an offensive, and therecords are a tribute to the scientific zeal of the surgeons working in theFifth U.S. Army hospitals.

TABLE 121.-Postmortem studies available and totalhospital battle casualty deaths studied,duringsurvey period, 1 January 1944-2 May 1945

Period	Gross findings available		Microscopic reports available		Total number of hospital battle casualty deaths studied¹
Period	Number	Percent	Number	Percent	Total number of hospital battle casualty deaths studied¹
1944
January-March	171	32.3	37	7.0	529
April-July	254	52.7	119	24.7	482
August-December	180	63.4	99	34.9	284
1945
January-May	128	82.6	94	60.6	155
Total	733	50.6	349	24.0	1,450

¹Includes records of 39 casualties who were DOA ata hospital.

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FIGURE 259.-95th Evacuation Hospital,Monghidoro, Italy.

It may be assumed that the 1,411 hospital battle casualtydeaths studied are truly representative of the total of 1,631 who (according toMTOUSA MD Form 86f) died in Fifth U.S. Army hospitals. Beginning with 1 January1944, General Martin requested submission of a complete record on all battlecasualties dying in Fifth U.S. Army hospitals. From 1 January 1944 to 2 May1945, the Adjutant General's "Wound Classification Report" submittedby the hospitals listed 58,677 battle casualty admissions and 1,562 battlecasualty deaths in hospitals. These figures are lower than those reported on theMTOUSA MD Form 86f. From the latter, the figure for battle casualty hospitaladmissions is 63,024 and for battle casualty hospital deaths, 1,631. Theselarger figures have been used in setting 86.5 percent as the portion studied ofall the hospital battle casualty deaths and have been correspondingly reducedwhen calculating percentage mortalities. In calculating percentages of totalbattle 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 86finclude the injured in action as well as the WIA and the KIA casualties. Of thedeaths studied, only a few who had crush injuries might be regarded as injuredrather than as wounded in action. All of the casualties (20) due to crushinjuries resulted from falling stones or bricks set in motion by the explosionof

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TABLE 122.-Correction of total battlecasualty admission figures to agree with proportion of totaldeaths analyzed, by survey period, 1 January 1944-2 May 1945

Survey period	Battle casualty deaths				Battle casualty admissions¹
	Reported¹ (number)	Studied²			Uncorrected (number)	Corrected (number)
	Reported¹ (number)	Number	Percent	Correction factor	Uncorrected (number)	Corrected (number)
1944
January-March	570	522	91.6	8.4	14,498	13,282
April-July	542	466	86.0	14.0	23,111	19,876
August-December	332	275	83.0	17.0	16,221	13,464
1945
January-May	187	148	79.2	20.8	9,194	7,282
Total	1,631	1,411	86.5	13.5	63,024	53,904

¹Data obtained from MTOUSA MD Form 86f.
²Excludes records of 39 casualties who were DOA at a hospital.

an enemy shell, and most of these casualties had wounds in addition to thecrush injury. It may be said, then, that the deaths studied represent aconsiderably larger percentage of WIA casualties who died than is indicated bythe percentage of 86.5 percent which is based upon the total (1,631) of woundedand injured in action who died in Fifth U.S. Army hospitals during the periodstudied. The breakdown of injured in action and wounded in action is notavailable either for hospital battle casualty admissions or for the totalresulting from the sum of the Adjutant General's figures on wounded in actionplus killed in action.

The 39 records of battle casualties DOA at a hospital comprise all therecords submitted on this class of deaths. Statistics are not available todetermine their percentage of the entire group of DOA's. Most of them wereunquestionably patients who, when seen by the last medical officer, wereexpected to reach the hospital alive. The DOA group has been included in thetables on wound classification and causes of death and, in many instances, hasbeen singled out for individual study as compared to the group of casualties whodied shortly after admission, before anesthesia, during anesthetic induction,during primary surgery, and after primary surgery. The cases have not beenincluded in tables dealing with hospital battle casualty deaths or in any of thepercentage tables based on hospital battle casualty admissions or the total ofwounded in action plus killed in action.

The information recorded in the tables of this report was first recorded incode form so that it might be transferred to machine records cards. Study of thecases 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

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FIGURE 260.-Capt. James W. Culbertson, MC,(right) obtaining information from hospital personnel concerning battlecasualties.

over 3 months. Col. Howard E. Snyder, MC, (fig. 261) thenstudied each case and checked the recorded data.²Each item was carefully weighed, matters calling for opinion werediscussed, and all questionable data were recorded as questionable. Thecompleted machine records cards were checked by hand for accuracy. ColonelSnyder and Captain Culbertson, with their clerical assistants, did all machinecounting and recording of data. Many checks were made on the validity of themachine tabulations. It is considered that the margin of error in this methodwas 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 casualtiesas related to hospital admission, anesthesia, and surgery. With experience andimprovement in the preparation of battle casualties for surgery, the number ofthose dying before anesthesia decreased throughout the period covered in thereport. When one compares the distribution of hospital deaths during the varioustime

²More data were accumulated than are presented in this chapter. In the original report, figures on timelags are available in all cases in which the information was in the record. Studies on all cases with nephropathies, fat embolisms, shock, thoracoabdominal wounds have been made. These studies are comparable in scope to that study on cases with intra-abdominal wounds which is presented in this report. It is hoped that the statistical information in the complete preliminary report will be of value to those studying and writing upon war surgery.-H. E. S. and J. W. C.

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FIGURE 261.-Col. Howard E. Snyder, MC,Surgical Consultant, Fifth U.S. Army, at the time the original report wascompiled.

periods to the total hospital battle casualty admissions(table 124), there is a consistent reduction in the percentage of those dyingbefore, during, and after anesthesia. Casualties at the Anzio beachhead wereincluded in the first two periods of the survey (January-March 1944; April-July1944) and unquestionably increased the percentage of those dying beforeanesthesia and the total hospital battle casualty mortality in the first twoperiods. The reduction in the latter mortality figure from 3.9 percent in thefirst period to 2.0 percent in the last is dependent on more than the Anziocasualties. The reduction in the percentage of those dying before anesthesia isin part due to the general adoption of improved methods of resuscitation and toa more available supply of blood. A hospital battle casualty mortality rate isinfluenced not only by the hospital's proximity to the battlefront but also bythe quality of care administered the wounded who reach it alive.

Morrissey has called attention to the direct relationship ofthe percentage mortality of battle casualties admitted to hospitals, thepercentage mortality of battle casualties admitted to hospitals and dying beforeanesthesia, and the percentage hospital battle casualty deaths comprised of thetotal who die of wounds (includes KIA) (table 125). He has shown that the latterpercentage varies widely. At Anzio, 16 percent of all battle casualty deathsoccurred in hos-

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TABLE 123.-Distribution of 1,450 deaths>¹as related to hospital admission, anesthesia, and surgery,during survey period, 1 January 1944-2 May 1945

Survey period	Dying on admission²		Died before anethesia³		Died during anesthetic induction		Died during primary surgery		Died after primary surgery		Total deaths
Survey period											Total deaths
	Number	Percent	Number	Percent	Number	Percent	Number	Percent	Number	Percent
1944

January-March	27	5.2	157	30.1	8	1.5	20	3.8	310	59.4	522
April-July	27	5.8	108	23.2	3	.6	25	5.4	303	65.0	466
August-December	12	4.4	48	17.4	4	1.5	19	6.9	192	69.8	275
1945

January-May	8	5.4	24	16.2	1	.7	11	7.4	104	70.3	148
Total	74	5.3	337	23.9	16	1.1	75	5.3	909	64.4	1,411

¹Excludes 39 DOA casualties. Theirdistribution was as follows: For the January-March 1944 period, 7; forApril-July 1944, 16; for August-December 1944, 16; for August-December 1944, 9;and for January-May 1945, 7.
²Lived less than an hour.
³Excludes those dying on admission.

TABLE 124.- Percentof 1,411 hospital deaths studied to total battle casualty hospital admissions(53,904), during survey period, 1 January 1944-2 May 1945

Survey period	Hospital deaths¹			Battle casualty hospital admissions²
Survey period	Total studied	Before anesthesia³	During anesthesia or surgery⁴	Total	Died before anesthesia	Died during anesthesia or surgery	Died in Army hospitals
1944	Number	Percent	Percent	Number	Percent	Percent	Percent
January-March	522	35.3	5.3	13,282	1.39	0.21	3.9
April-July	466	29.0	6.0	19,876	.68	.14	2.3
August-December	275	21.8	8.4	13,464	.44	.17	2.0
1945
January-May	148	21.6	8.1	7,282	.44	.16	2.0
Total	1,411	29.1	6.4	53,904	.75	.16	2.6

¹Excludes 39 DOA casualties.
²Corrected to allow for percentage of deaths not studied during eachperiod. (See table 122.)
³From table 123, includes those dying on admission.
⁴From table 123.

pitals (hospital mortality, 5.7 percent). In May 1944, 4.21percent of all battle casualty deaths occurred in hospitals (hospital mortality,1.7 percent). In June 1944, 15 percent of all battle casualty deaths were inhospitals (hospital mortality, 2.8 percent). In October 1944, 7.65 percent ofall battle casualty deaths were in hospitals (hospital mortality, 2.1 percent).When evacuation of the wounded to the forward hospital (fig. 262) is easilyaccomplished,

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FIGURE 262.-Location of field hospitalplatoon used as a forward surgical unit before the breakthrough into the PoValley.

the hospital mortality rises. Thus, hospital mortality tendsto vary inversely with the percentage who are killed in action or who die ofwounds before reaching a hospital. However, as is shown in table 125, there hasbeen a steady, gradual decrease in the percentage which deaths occurring duringand after surgery comprise of total battle casualty deaths. Table 124 shows aslight increase throughout the four periods in the percentage which deathsduring surgery comprise of the deaths studied but a decrease in the percentagethese deaths comprise of battle casualties admitted to hospitals.

The simple classification of cases by region of principalwound in table 126 is presented for comparison with similar tables on hospitalbattle casualty admissions and deaths which were available for all of theTunisian, Sicilian, and Italian campaigns.

Table 127 lists battle casualty hospital deaths according toprincipal wound groups. It was found that in only 33.3 percent of the casualtiesstudied 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 thebody. Many of the 33.3 percent had multiple wounds, but these wounds werelimited to only one of the anatomic regions.³

³(1) A more detailed breakdown of the cases listed in table 127 is presented in tables 1 and 2, appendix D (p. 807). Table 1 presents the distribution of associated wounds as related to the region of the principal wound; table 2 presents the regional distribution of principal and associated wounds with the number of cases exhibiting each. (2) A further-clarification of the three wound classes in table 127, involving intrathoracic, thoracoabdominal, and combined intraabdominal and intrathoracic wounds, is presented in appendix E (p. 811).

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TABLE 125.-Demonstration of effect ofincreased efficiency of evacuation from forward areas on hospital mortality (anincrease) and the remaining favorable trend after exclusion of those cases¹dying before anesthesia

Category	January- March 1944	April- July 1944	August- December 1944	January- May 1945
Killed, wounded, and injured in action...number...	24,351	32,026	22,469	12,556
Killed in action plus died of wounds²...do...	5,042	6,366	4,234	2,506
Mortality of the killed, wounded, and injured in action...percent...	20.70	19.88	18.84	19.96
Battle casualties admitted to hospitals...number...	14,498	23,111	16,221	9,194
Battle casualties dying in hospitals...do...	570	542	332	187
Mortality of battle casualties admitted to hospitals...percent...	3.94	2.34	2.05	2.04
Total battle casualty deaths dying in hospitals...percent...	11.3	8.5	7.8	6.8
Hospital battle casualty deaths who died before anesthesia...percent...	35.3	29.0	21.8	21.6
Hospital battle casualty deaths who died after reaching anesthesia...percent...	7.3	6.2	6.14	5.3
Total killed, wounded, and injured in action who died after reaching anesthesia...percent...	1.515	1.200	1.160	1.050

¹A variable quantity influenced byconditions affecting efficiency of evacuation to hospitals as well as byprofessional care before and after admission.
²Does not include those few deaths which occurred in base hospitals.
Source: History of Fifth Army Medical Service, 1945. [Official record.]

TABLE 126.- Distribution of battle casualtyhospital deaths (1,450 cases), by region of principal wound

Region of principal wound	Number of cases	Percent of cases
Abdomen	543	37.4
Head	297	20.5
Chest	277	19.1
Lower extremity	145	10.0
Spine	27	1.9
Neck	25	1.7
Upper extremity	14	.9
Face and jaws	8	.6
Unclassified multiple wounds	114	7.9
Total	1,450	100.0

Table 127 may be compared with the distribution of woundsamong all battle casualties admitted to Fifth U.S. Army hospitals during theperiod of 1 August 1944 to 2 May 1945 (table 128). Intra-abdominal woundscomprise only 2.84 percent of battle casualties admitted to a hospital but 20percent of them died and these comprise 28.1 percent of all hospital battlecasualty deaths.

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TABLE 127.- Distribution of battle casualtyhospital deaths (1,450 cases), by principal wound

Principal wound	Total cases		Cases without associated wounds
Principal wound	Number	Percent	Number	Percent
Intra-abdominal¹	408	28.1	131	32.1
Intracranial	297	20.5	138	46.5
Thoracoabdominal²	212	14.6	98	46.2
Intrathoracic2	138	9.5	37	26.8
Lower extremity, with bone involvement	³114	7.8	⁴49	43.0
Unclassified, multiple wounds	114	7.8	---	---
Combined intra-abdominal and intrathoracic²	59	4.1	7	11.9
Lower extremity, soft tissue only	31	2.2	14	45.2
Intravertebral	27	1.9	1	3.7
Cervical	25	1.0	5	20.0
Upper extremity, with bone involvement	⁵10	.7	2	20.0
Maxillofacial, with bone involvement	8	.6	1	12.5
Upper extremity, soft tissue only	4	.3	---	---
Abdominal wall	3	.2	---	---
Total	1,450	100.0	483	33.3

¹A more detailed classification islisted in appendix D, p. 807.
²A more detailed classification is listed in appendix E, p. 811.
³Includes 43 traumatic amputations.
⁴Includes 17 traumatic amputations.
⁵Includes 2 traumatic amputations.

TABLE 128.-Distribution of 20,747 Americanbattle casualties admitted to Fifth U.S. Armyhospitals, 1 August 1944-2 May 1945, by principal woundgroup

Principal wound	Percent of all battle casualty admissions	Percent that died
Intra-abdominal	2.84	20.0
Thoracoabdominal plus intra-abdominal and intrathoracic	1.66	20.4
Superficial abdominal	.74	.0
Intrathoracic	4.64	7.8
Superficial thoracic	3.73	.2
Intracranial	1.95	26.00
Scalp	3.77	.0
Lower extremity:
Soft tissue and bone	9.35	1.74
Soft tissue only	32.48	.25
Upper extremity:
Soft tissue and bone	6.25	.28
Soft tissue only	19.30	.02
Neck	2.07	.87
Spine	.94	7.10
Maxillofacial:
Soft tissue only	4.68	.29
Bone and soft tissue	1.22	1.50
Eye and ear	2.00	.00
Other	2.30	.55

NOTE.-0.0 indicates a rate of more than zero but less than0.05, and 0.00 a rate of more than zero but less than 0.005.

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The intra-abdominal, intrathoracic, thoracoabdominal,combined intra-abdominal and intrathoracic, and intracranial wounds compriseonly 11.09 percent of hospital battle casualty admissions, and yet they accountfor 76.8 percent of all hospital battle casualty deaths. Table 129 relates the1,411 hospital battle casualty deaths to the total hospital battle casualtyadmissions during the survey period.

TABLE 129.-Hospital battle casualty deaths listed asto principal wound with percentage ofhospital battle casualty admissions

Principal wound	Number of deaths¹	Percent of total² hospital battle casualty admissions (53,904)
Intra-abdominal	402	0.745
Intracranial	288	.534
Thoracoabdominal	210	.389
Intrathoracic	131	.241
Super extremity (bone involvement)	110	.204
Unclassified, multiple wounds	106	.196
Combined intra-abdominal and intrathoracic	57	.105
Lower extremity, soft tissue only	30	.055
Intravertebral	27	.050
Cervical	25	.046
Upper extremity (bone involvement)	10	.018
Maxillofacial	8	.014
Upper extremity, soft tissue only	4	.007
Abdominal wall	3	.005
Total	1,411	2.61

¹Does not include 39 DOA casualties.
²Figure of total 63,024 admissions corrected to allow for 13.5percent of hospital battle casualty deaths not studied.

The type of causative agent as related to the principal woundis listed in table 130. Small arms accounted for approximately 15.11 percent ofthe 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 ofdeath and the hospital admission, anesthesia, and surgery.

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TABLE 130.-Distribution of 1,450casualties, by causative agent as related to principal wound

Principal wound	Total casualties	Bullet			High explosive						No record of causative agent	Casualties with-
Principal wound	Total casualties	Unclas- sified	Rifle	Machine gun	Unclas- sified	Shell	Mine	Booby- trap	Bomb	Blast	No record of causative agent	Pene- trating wound¹	Perforat- ing wound¹
Intracranial	297	19	8	6	37	181	10	---	17	2	17	199	42
Intra-vertebral	27	2	2	2	2	14	---	---	2	---	3	19	5
Maxillofacial	8	---	---	1	1	4	---	---	---	1	1	4	1
Cervical	25	3	---	2	4	13	1	---	2	---	---	16	1
Intra- thoracic	138	20	1	9	12	79	2	---	4	1	10	94	33
Thoraco-abdominal	212	35	7	7	11	130	10	---	8	---	4	152	67
Combined intra-abdominal and intrathoracic	59	2	1	---	8	37	4	---	3	2	2	47	11
Intra-abdominal	408	54	11	15	40	254	9	---	12	1	12	287	126
Abdominal wall only	3	---	---	---	---	3	---	---	---	---	---	2	---
Upper extremity:
Soft tissue only	4	---	---	---	---	2	---	---	---	---	2	3	---
Bone and soft tissue	10	---	---	---	4	6	---	---	---	---	---	5	1
Lower extremity:
Soft tissue only	31	5	---	1	5	14	2	---	2	1	1	12	7
Bone and soft tissue	114	2	---	2	21	59	19	---	7	---	4	47	21
Unclassified, multiple	114	1	1	---	15	65	13	2	10	2	5	78	17
Total	1,450	143	31	45	160	861	70	2	67	10	61	965	332

¹Cases of blast, crush, and mutilatinginjury could not be classified in this manner, and number is less than total of1,450.

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TABLE 131.-Distribution of 1,450 battle casualtydeaths as related to hospital admission, anesthesia, and surgery, by principal wound

Principal wound	DOA	Dying on admission¹	Died before anesthesia²	Died during anesthetic induction	Died during primary surgery	Died after primary surgery
Intra-abdominal	6	12	45	8	20	317
Intracranial	9	17	142	---	6	123
Thoracoabdominal	2	3	20	2	29	156
Intrathoracic	7	13	35	2	8	73
Lower extremity, bone and soft tissue	4	14	18	---	5	73
Unclassified multiple	8	7	45	2	3	49
Combined intra-abdominal and intrathoracic	2	3	6	1	2	45
Lower extremity, soft tissue only	1	2	5	---	---	23
Intravertebral	---	---	10	---	---	17
Cervical	---	2	5	---	2	16
Upper extremity, bone and soft tissue	---	1	2	---	---	7
Maxillofacial	---	---	---	1	---	7
Upper extremity, soft tissue only	---	---	4	---	---	---
Abdominal wall only	---	---	---	---	---	3
Total	39	74	337	16	75	909

¹Lived less than 1 hour.
²Excludes the DOA cases and those casualties who lived less than 1hour.

CAUSES OF DEATH

General Observations

Certain problems were encountered in the classification andarrangement of this material. The Adjutant General of the Fifth U.S. Army andThe Adjutant General of the U.S. Army report battle casualty deaths as"killed in action" or "died of wounds" (the latter includesthose dying of injuries incurred in action). Hospitals report deaths accordingto a classification of principal wounds. Generally speaking, all battlecasualties who die are said to die of wounds or injuries incurred in action. Allof the cases reported in this study may be said to have died either of wounds orof injuries incurred in action against the enemy. Table 132 classifies the casesas to region of primary trauma leading to death. This classification iscomparable 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 poplitealartery 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 awound of

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TABLE 132.- Distribution of battle casualty hospital deaths (1,450 cases) during survey period, 1 January 1944-2 May 1945, by region of primary trauma leading to death

Region of primary trauma	January-March 1944		April-July 1944		August-December 1944		January-May 1945		Total
Region of primary trauma	Number	Percent	Number	Percent	Number	Percent	Number	Percent	Number	Percent
Shock¹	183	34.6	192	39.9	93	32.7	55	35.5	523	36.1
Intracranial	73	13.7	71	14.7	48	16.9	42	27.1	234	16.1
Thoracic	45	8.4	45	9.4	47	16.5	21	13.6	158	10.9
Abdominopelvic	30	5.6	59	12.3	47	16.5	18	11.6	154	10.6
Extremity	32	6.0	8	1.7	3	1.1	2	1.3	45	3.1
Spinal	6	1.1	1	.2	9	3.2	3	1.9	19	1.3
Miscellaneous (general)	5	.9	3	.4	3	.1	---	---	11	.8
Cervical	1	.6	1	.2	---	---	---	---	2	.1
Maxillofacial	---	---	1	.2	---	---	---	---	1	.1
Undetermined, unclassified	154	29.1	101	21.0	34	12.0	14	9.0	303	20.9
Total	529	100.0	482	100.0	284	100.0	155	100.0	1,450	100.0

¹Generalized conditions involving more than oneregion.

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 isthat the immediate or precipitating cause of death is shock (peripheral vascularfailure).

While fully aware of the controversial nature of the subject, the decisionwas made to include the uncorrected state of shock as an immediate orprecipitating cause of death, along with other more specific, standarddiagnoses. It may be contended, of course, that such patients actually die oftheir wounds and the severity of the trauma attending them and that the shockwhich is present is a syndrome reflecting a profound pathologic alteration ofnormal hemodynamics and is not an acceptable diagnosis. However, in this study,as just stated, each case has been classified as to primary trauma leading todeath (the conventional primary or basic diagnosis), and the liberty ofemploying the concept of the state of shock as a "diagnosis" for theimmediate or precipitating cause of death (the conventional secondary diagnosis)allows for a more complete classification of the causes of death for comparisonand study. This sets in relief that important group of cases which succumbedfrom the gravity of their wounds in a state of uncontrolled shock. It seems thatthis group of cases is worthy of the special attention afforded by such aclassification.

Shock was selected as the immediate cause of death in 523 cases in thisseries. A special study was made on this group and is presented on page 511. Thecriteria used in naming shock as an immediate cause of death are discussed thereand are apparent in the information tabulated.

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"Neural trauma and/or intracranial hemorrhage orclot" was listed as the immediate cause of death in 212 cases and is secondon the list of the immediate causes of death, as is shown in tables 133 and 134and in the tabulation which is to follow. The relative importance as a lethalfactor of the brain damage produced by the missile and the damage produced by anexpanding intracranial hematoma was often difficult to determine. It seemedunwise, considering the available information and the qualifications necessaryfor evaluation, to attempt to separate these cases into two groups. It may bementioned here that only 15 cases in whom the principal wound was intracranialwere listed as dying of shock, while 210 were listed as dying of neural traumaor clot. (All 235 cases in these two categories were listed also under theheading "Primary trauma leading to death, intracranial.")Nephropathies were third on the list, and their incidence was relativelyconstant 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 andis therefore apparent rather than real.

	Number of cases		Number of cases
Immediate cause of death:		Immediate cause of death-Con.
Shock	523	Pulmonary blast and other trauma	2
Neural (brain) trauma and/or intracranial hemorrhage or clot	212	Ventricular arrest	2
Pigment nephropathy	68	Abscess, intracranial	1
Peritonitis	65	Infarction, brain and lung	1
Clostridial myosits	51	Mediastnial hemorrhage	1
Pneumonia	49	Mediastinitis	1
Fat embolism	27	Meningitis, spinal	1
Thrombotic embolism	20	Pneumonitis	1
Spinal cord trauma	16	Respiratory failure, cause undetermined	1
Tracheobronchial obstruction:		Sepsis unclassified, abdominal	1
Aspirated vomitus	11	Sepsis unclassified, extremity	1
Blood and mucus	11	Septicemia	1
Cerebral ischemia	8	Thoracoabdominal trauma, unclassified	1
Anesthetic agent	7	Transfusion reaction	1
Empyema thoracis	7	Other intra-abdominal condition	2
Intracranial blast trauma alone	5	Other intracranial condition	1
Cellulitis (extraperitoneal)	4	Undetermined thoracic condition	12
Myocardial decompensation	4	Undetermined intra-abdominal condition	4
Coronary occlusion	3	Undetermined abdominal wall	1
Pulmonary blast trauma alone	3	Undetermined intracranial condition	2
Respiratory obstruction above trachea	3	Undetermined, unclassified	303
Abscess, intra-abdominal	2	Total	1,450
Air embolism	2
Infarction of lung	2
Intestinal obstruction	2
Intracranial blast and other trauma	2
Meningitis, intracranial	2

488

TABLE 133.-Distribution of 1,450 battle casualty deaths¹during survey period, 1 January1944-2 May 1945, by cause of death

Cause of death	January-March 1944		April-July 1944		August-December 1944		January-May 1945		January 1944 through May 1945
Cause of death	Number	Percent	Number	Percent	Number	Percent	Number	Percent	Number	Percent
Shock	183	34.6	194	40.3	91	32.0	55	35.5	523	36.1
Neural trauma and/or intracranial hemorrhage or clot	65	12.3	66	13.7	45	15.8	36	23.2	212	14.7
Nephropathy	9	1.7	25	5.2	26	9.2	8	5.2	68	4.7
Peritonitis	13	2.5	26	5.4	19	6.7	7	4.5	65	4.5
Clostridial myositis	35	6.6	11	2.3	4	1.4	1	.6	51	3.5
Pneumonia	20	3.8	6	1.2	17	6.0	6	3.9	49	3.4
Fat embolism	5	.9	9	1.9	9	3.2	4	2.6	27	1.9
Thrombotic embolism	5	.9	12	2.5	1	.4	2	1.3	20	1.4
Spinal cord trauma	6	1.1	1	.2	6	2.1	3	1.9	16	1.1
Tracheobronchial obstruction:
Aspirated vomitus	3	.6	1	.2	3	1.1	4	2.6	11	.8
Blood and mucus	1	.2	4	.8	3	1.1	3	1.9	11	.8
Cerebral ischemia	2	.4	1	.2	2	.7	3	1.9	8	.6
Others in which immediate cause of death is known	28	5.3	25	5.2	24	8.4	9	5.9	86	5.6
Remainder in which immediate cause of death is undetermined, unclassified	154	29.1	101	20.9	34	11.9	14	9.0	303	20.9
Total	529	100.0	482	100.0	284	100.0	155	100.0	1,450	100.0

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 thethird 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, itfell to the bottom of the list, with only one death attributed to it, comprising0.6 percent of the deaths studied, and only 0.01 percent of all battlecasualties admitted to hospitals. The educational program concerning clostridialmyositis 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 allwounds, the more liberal use of blood, and the advent of the extensive use ofpenicillin were important factors in effecting this striking reduction inmortality and the corresponding reduction in the incidence.

Peritonitis tended to show a slight increase in itspercentage of the total battle casualty admissions and a more pronouncedincrease in its percentage of the deaths studied. There are two factors whichmay have contributed. First is the reduction in mortality from shock,clostridial myositis, extremity wounds,

489

TABLE 134.-Distribution of 1,450 battle casualtydeaths, showing percent of the total battle casualty admissions (53,904)¹during surveyperiod, 1 January 1944-2 May 1945, bycause of death

Cause of death	January-March 1944	April-July 1944	August-December 1944	January-May 1945	January 1944 through May 1945
Shock	1.38	0.98	0.676	0.750	0.960
Neural trauma and/or intracranial hemorrhage or clot	.49	.35	.334	.490	.390
Peritonitis	.068	.126	.193	.110	.125
Clostridial myositis	.280	.055	.030	.010	.094
Pneumonia	.160	.030	.126	.080	.090
Fat embolism	.040	.040	.067	.050	.050
Thrombotic embolism	.040	.060	.010	.030	.040
Spinal cord trauma	.050	.005	.050	.040	.030
Tracheobronchial obstruction:
Aspirated vomitus	.020	.005	.020	.050	.020
Blood and mucus	.010	.020	.020	.040	.020
Cerebral ischemia	.020	.005	.015	.040	.015

¹Corrected to allow for the percentage of hospital battle casualtydeaths not studied in each period.

and unclassified wounds in the course of the 17 monthscovered by the study. This has led to a relative increase in peritonitis deaths,deaths from intracranial wounds, and other wounds or complications, theincidence of which was more or less inevitable. The second factor is theincrease in the percentage of autopsies performed which probably accounts forthe apparent but slight increase in the number of peritonitis deaths as comparedto hospital battle casualty admissions.

The only striking variation in mortality from pneumonia is inthe April-July 1944 period, in which pneumonia deaths comprised only 1.2percent of the deaths studied as compared to the average of 3.4 percent for allfour periods. It is the only one of the four periods which did not includewinter months.

Tables 135, 136, and 137 compare the region of principalwound, the immediate cause of death, and the region of primary trauma. Attentionis directed to the incidence of fat embolism. This diagnosis was not recordedexcept when microscopic reports indicated large amounts of fat in the pulmonarysections 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 22additional cases in which it was listed as a contributory condition rather thanas the immediate cause of death.

Thrombotic embolism and tracheobronchial obstruction fromaspirated vomitus, blood, or mucus appear quite prominently in the leadingcauses of death. Their relative incidence showed a definite increase and theactual incidence perhaps a slight increase in spite of recognition of theirimportance and the inauguration of prophylactic measures early in the campaign.

490

TABLE 135.-Comparison of principal woundwith region of immediate cause of death (1,450 cases)

Anatomic region	Region of principal wound in-		Region of immediate cause of death in-
Anatomic region	Cases (number)	Percent of cases studied	Cases (number)	Percent of cases studied
Abdominal	543	37.5	154	10.6
Intracranial	297	20.5	234	16.1
Thoracic	277	19.1	158	10.9
Extremity	159	11.0	45	3.1
Intravertebral	27	1.8	19	1.3
Cervical	25	1.7	2	.1
Maxillofacial	8	.5	1	.1
Unclassified	¹114	7.9	²303	20.9
General³	---	---	11	.8
Shock	---	---	523	36.1
Total	1,450	100.0	1,450	100.0

¹Multiple wounds.
²Cause of death undetermined.
³More than one region involved by cause of death, excluding shock.

TABLE 136.- Region of immediate cause of death as related to region of principal wound (1,450 cases)

Principal wound	Abdom- inal	Cervical	Extrem- ity	Intra- cranial	Maxillo- facial	Spinal	Thoracic	General¹	Shock	Undetermined, unclassified
Intracranial	2	---	3	221	---	1	15	---	15	40
Intravertebral	---	---	---	---	---	16	4	---	4	3
Maxillofacial	---	---	---	---	---	---	3	---	1	4
Cervical	1	2	---	4	---	---	4	---	11	3
Intrathoracic	3	---	1	3	---	---	37	1	70	23
Thoracoabdominal	25	---	---	1	1	---	20	1	118	46
Combined intra-abdominal and intrathoracic	14	---	---	1	---	---	7	1	25	11
Intra-abdominal	89	---	7	---	---	---	39	4	178	91
Abdominal wall only	1	---	---	---	---	---	1	---	---	1
Upper extremity:
Soft tissue only	1	---	---	---	---	---	---	---	2	1
Bone and soft tissue	---	---	1	---	---	---	---	1	3	5
Lower extremity:
Soft tissue only	5	---	8	---	---	1	3	1	9	4
Bone and soft tissue	8	---	22	1	---	---	15	2	41	25
Unclassified, multiple	5	---	3	3	---	1	10	---	46	46
Total	154	2	45	234	1	19	158	11	523	303

¹Involving more than one region, a miscellaneousgroup, excluding shock.

491

TABLE 137.- Region of primary trauma leading to death, by period

Primary trauma	January-March 1944		April-July 1944		August-December 1944		January-May 1945		Total
Primary trauma	Number	Percent	Number	Percent	Number	Percent	Number	Percent	Number	Percent
Abdominopelvic	124	23.5	131	27.2	80	28.2	33	21.3	368	25.4
Intracranial	97	18.3	81	16.8	57	20.1	46	29.7	281	19.4
Thoracoabdominal	62	11.7	74	15.3	43	15.1	23	14.8	202	13.9
Extremity	83	15.7	58	12.0	28	9.9	9	5.8	178	12.3
Unclassified, multiple	83	15.7	55	11.4	25	8.8	12	7.7	175	12.1
Thoracic	44	8.3	49	10.2	30	10.5	11	7.1	134	9.2
Combined thoracic and abdominal	18	3.4	17	3.6	10	3.5	8	5.2	53	3.7
Cervical	8	1.5	10	2.1	2	.7	6	3.9	26	1.8
Spinal	7	1.3	4	.8	8	2.8	6	3.9	25	1.7
Maxillofacial	1	.2	3	.6	1	.4	1	.6	6	.4
Undetermined¹	2	.4	---	---	---	---	---	---	2	.1
Total	529	100.0	482	100.0	284	100.0	155	100.0	1,450	100.0

¹Record inadequate indescription of wounds.

Tables 138 through 149 deal with the total reported incidenceof immediate and contributing causes of death. In this report, they are the bestsource of information regarding the incidence of any one condition. All thefigures in the column under "Immediate cause of death" representevident or confirmed incidence. The figures in the middle column represent bothevident and suspected evidence, but in every instance they are separated andproperly identified by the index column. The same applies to the total figuresin the last column.

TABLE 138.- Total reported incidence of shock in 1,450battle casualty deaths

Etiology or type of shock	Immediate cause of death	Contributory or associated condition	Total reported¹ incidence
Cardiorespiratory embarrassment plus trauma and hemorrhage	147	135	282
Cardiorespiratory embarrassment plus trauma and hemorrhage plus contamination or sepsis	72	58	130
Contamination or sepsis plus trauma and hemorrhage	120	186	306
Trauma and hemorrhage	182	370	552
Type undetermined	2	1	3
Total	523	750	1,273

¹Probably somewhat lower than the actual incidence.

492

The figures are believed to be lower than the actualincidence inasmuch as they represent only the reported incidence, and inasmuchas the records at times are not complete. The incidence figures on shock areperhaps nearer the actual than most of the other figures, because manyindications of the presence of shock may be found in the record when it ispresent.

TABLE 139.- Total reported incidence of intracranialconditions in 1,450 battle casualty deaths

Intracranial condition	Immediate cause of death	Contributory or associated condition	Total reported¹ incidence
Abscess	1	10	11
Blast trauma:
Evident	7	17	24
Suspected	---	29	29
Cerebral death suspected	---	57	57
Encephalomalacia	---	60	60
Fungus, cerebral, septic	---	2	2
Hygroma	---	4	4
Ischemia	8	14	22
Meningitis	2	7	9
Trauma and/or hemorrhage, evident, unclassified²	212	155	367
Intracranial trauma,² unclassified, suspected	---	16	16
Other	1	---	1
Undetermined	2	---	2
Respiratory failure, cause undetermined	1	---	1
Total	234	371	605

¹Probably somewhat lower than the actualincidence.
²As distinguished from blast trauma.

TABLE 140.- Total reported incidence ofshock in 1,450 battle casualty deaths

Shock condition	Immediate cause of death	Contributory or associated condition	Total reported¹ incidence
Corrected by therapy	---	339	339
Suspected, not proved	---	²76	76
Successful correction doubtful	---	207	207
Uncorrected	523	128	651
Total	523	750	1,273

¹Probably somewhat lower than actual incidence.
²In an additional 128 cases, shock was suspected as being acontributory cause of death.

493

TABLE 141.-Total reported incidence of maxillofacialconditions in 1,450 battle casualty deaths

Maxillofacial condition	Immediate cause of death	Contributory or associated condition	Total reported¹ incidence
Trauma	---	182	182
Hemorrhage	---	9	9
Respiratory obstruction:

Due to plugging of airway	1	2	3
Due to edema or hemorrhage	---	2	2
Sepsis	---	4	4
Total	1	199	200

¹Probably somewhat lower than the actual incidence.

TABLE 142.- Total reported incidence of cervicalconditions in 1,450 battle casualty deaths

Cervical condition	Immediate cause of death	Contributory or associated condition	Total reported¹ incidence
Trauma	---	108	108
Hemorrhage	---	27	27
Laceration, fatal, carotid, or subclavian artery	---	²4	4
Respiratory obstruction:

Due to edema or hematoma	2	10	12
Due to plugging of airway	---	9	9
Sepsis	---	3	3
Total	2	161	163

¹Probably somewhat lower than the actual incidence.
²Immediate cause of death, listed as shock.

TABLE 143.-Total reported incidence of intravertebralconditions in 1,450 battle casualty deaths

Intravertebral condition	Immediate cause of death	Contributory or associated condition	Total reported¹ incidence
Trauma	16	88	104
Hematomyelia	---	19	19
Hemorrhage	---	13	13
Meningitis	1	1	2
Transection of cord:
Complete	---	²24	24
Partial	---	11	11
Total	17	156	173

¹Probably somewhat lower than the actual incidence.
²Includes cases from those in whom the immediate cause of death wasintravertebral trauma.

494

TABLE 144.- Total reported incidence of extremity conditions in 1,450 battle casualty deaths

Extremity condition	Immediate cause of death	Contributory or associated condition	Total reported¹ incidence
Trauma, unclassified	---	669	669
Clostridial myositis of extremity:

Evident	²44	²8	52
Suspected	---	²28	28
Crushing trauma	---	3	3
Hemorrhage	---	142	142
Sepsis (not clostridial)	---	53	53
Sepsis, unclassified	1	---	1
Frostbite or immersion syndrome	---	8	8
Total	45	911	956

¹Probably somewhat lower than the actual incidence.
²Also included in clostridial infections (table 147).

TABLE 145.- Total reported incidence of thoracic conditions in 1,450battle casualty deaths

Thoracic condition	Immediate cause of death	Contributory or associated condition	Total reported¹ incidence
Trauma, unclassified	---	176	176
Thoracoabdominal trauma	1	14	15
Combined intra-abdominal and intrathoracic trauma	---	4	4
Atelectasis:
Severe	---	33	33
Slight or moderate	---	71	71
Blast trauma:
Evident	5	84	89
Suspected	---	77	77
Bronchial fistula:
Evident	---	21	21
Suspected	---	5	5
Cardiac trauma:
Evident	²2	31	33
Suspected	---	29	29
Continuing intrapleural hemorrhage	---	8	8
Coronary occlusion	3	---	3
Crushing trauma:
Evident	---	5	5
Suspected	---	1	1
Dilatation of heart:
Severe	---	28	28
Slight or moderate	---	61	61
Empyema:
Mild or moderate	---	17	17
Severe	7	6	13
Suspected	---	12	12
External hemorrhage from chest wall	---	2	2
Fat embolism, pulmonary:
Evident	³27	20	47
Suspected	---	65	65
Hemopneumothorax:
Evident	---	347	347
Suspected	---	61	61
Hydrothorax:
Severe	---	9	9
Slight or moderate	---	77	77
Infarction of lung	³3	³6	9
Intrapulmonary hemorrhage:
Mild or moderate	---	192	192
Severe	---	68	68
Suspected	---	36	36
Lung abscess	---	14	14
Mediastinal edema	---	5	5
Mediastinal emphysema	---	16	16
Mediastinal hemorrhage	1	29	30
Mediastinitis	1	4	5
Myocardial decompensation:⁴
Evident	4	112	116
Suspected	---	211	211
Other	---	14	14
Pleural contamination from abdomen, evident	---	22	22
Pneumonia:
Mild or moderate	---	100	100
Severe	49	22	71
Suspected	---	28	28
Pneumonitis	1	14	15
Pneumothorax without hemothorax	---	5	5
Pulmonary edema:
Severe	---	204	204
Slight or moderate	---	145	145
Purulent bronchitis	---	35	35
Subpleural emphysema	---	5	5
Tension pneumothorax:
Evident	---	18	18
Suspected	---	7	7
Thrombotic embolism, pulmonary:
Evident	³20	³14	34
Suspected	---	17	17
Tracheobronchial obstruction:
Aspirated vomitus	11	21	32
Blood and mucus	11	103	114
Suspected	---	25	25
Unrepaired wound and diaphragm	---	26	26
Ventricular arrest	2	---	2
Undetermined	12	---	12
Total	160	2,782	2,942

¹Probably somewhat lower than the actual incidence.
²Also included with coronary occlusions and raises the totalconditions to 160 rather than the 158 as listed in table 136.
³Also included with embolism, thrombosis, and infarction (table 148).
⁴Does not include the three cases of coronary occlusion.

TABLE 146.-Total reported incidence of abdominalconditions in 1,450 battle casualty deaths

Abdominal condition	Immediate cause of death	Contributory or associated condition	Total reported¹ incidence
Abdominopelvic trauma	---	147	147
Combined intra-abdominal and intrathoracic trauma	---	4	4
Thoracoabdominal trauma	---	14	14
Abscess:
Extraperitoneal	---	12	12
Intraperitoneal	2	15	17
Adrenal hemorrhage	---	15	15
Adrenal trauma	---	8	8
Adynamic ileus:
Mild or moderate	---	36	42
Severe	---	42	42
Suspected	---	1	1
Blast trauma:
Evident	---	26	26
Suspected	---	20	20
Cellulitis, mural and extraperitoneal	4	20	24
Clostridial myositis of trunk (abdominal):
Evident	²7	²4	11
Suspected	---	²10	10
Contamination from hollow viscus	^---	467	467
Crushing trauma:
Evident	---	6	6
Suspected	---	6	6
Evisceration:
Postoperative	---	7	7
Preoperative	---	78	78
Postoperative and preoperative	---	2	2
Gangrene of bowel:
Advanced	---	9	9
Early	---	13	13
Gastric dilatation	---	38	38
Hemorrhage, primary	---	499	499
Hemorrhage, recurrent or delayed	---	26	26
Hepatic degeneration, toxic	---	75	75
Hepatitis, epidemic:
Evident	---	7	7
Suspected	---	4	4
Hepatitis, septic, secondary to trauma:
Evident	---	18	18
Suspected	---	18	18
Inflammation of G-I tract	---	7	7
Intestinal obstruction (mechanical):
Mild or moderate	---	8	8
Severe	2	6	8
Suspected	---	3	3
Leaking suture line	---	8	8
Nephropathy, pigment:
Evident	68	31	99
Suspected	---	8	8
Nephropathy, toxic, degenerative	---	26	26
Operative wound infection	---	17	17
Other abdominal condition	2	23	25
Pancreatic:
Hemorrhage	---	6	6
Trauma	---	25	25
Peritonitis:
Mild or moderate	---	92	92
Severe	65	48	113
Suspected	---	63	63
Renal sepsis (parenchymal)	---	5	5
Renal trauma:
Evident	---	127	127
Suspected	---	11	11
Sepsis, abdominal, unclassified	1	---	1
Splenic degeneration, toxic	---	28	28
Splenomegaly	---	31	31
Unrepaired wound of hollow viscus³	---	33	33
Ureter traumatized or tied:
Evident	---	12	12
Suspected	---	3	3
Urinary tract sepsis	---	11	11
Undetermined abdominal wall condition	1	---	1
Undetermined intra-abdominal condition	4	---	4
Undetermined: contamination and/or hemorrhage suspected	---	86	86
Total	154	2,365	2,521

¹Probably somewhat lower than the actualincidence.
²Also reported with clostridial myositis (table 147).
³Recorded only for patients who had intraperitoneal surgery.

498

TABLE 147.-Total reported incidence of clostridialmyositis or cerebritis in 1,450 battle casualtydeaths

Clostridial infections	Immediate cause of death	Contributory or associated condition	Total reported¹ incidence
Clostridial myositis of extremity:

Evident	46	8	54
Suspected	---	28	28
Clostridial myositis or cerebritis of head, neck, or trunk:

Evident	5	4	9
Suspected	---	10	10
Total	51	50	101

¹Probably somewhat lower than the actual incidence.

TABLE 148.-Total reported incidence of embolism,infarction, and thrombosis in 1,450 battle casualty deaths

Pathological condition	Immediate cause of death	Contributory or associated condition	Total reported¹ incidence
Embolism, air:

Evident	2	2	4
Suspected	---	12	12
Embolism, fat:

Evident	27	22	49
Suspected	---	65	65
Embolism, thrombotic:
Evident	20	14	34
Suspected	---	17	17
Embolism, thrombotic, and infarction	---	5	5
Infarction alone	3	13	16
Infarction and thrombosis	---	9	9
Thrombosis alone:
Evident	---	35	35
Suspected	---	3	3
Total	52	197	249

¹Probably somewhat lower than theactual incidence.

499

TABLE 149.-Total reported incidence of miscellaneousconditions in 1,450 battle casualty deaths

Miscellaneous conditions	Immediate cause of death	Contributory or associated condition	Total reported¹ incidence
Anaphylaxis, suspected	---	2	2
Anemia, refractory or severe	---	13	13
Anesthetic agent:
Cause of death	7	---	7
Suspected	---	25	25
Blast death, suspected	---	29	29
Jaundice	---	24	24
Malnutrition, severe	---	10	10
Morphine poisoning:
Cause of death	---	---	---
Suspected	---	4	4
Other contributory conditions	---	2	2
Septicemia (excluding clostridial)	1	1	2
Transfusion reaction, severe	1	6	7
Respiratory failure, cause undetermined	1	---	1
Undetermined, unclassified	303	---	303
Total	313	116	429

¹Probably somewhat lower than theactual incidence.

Detailed Observations⁴

In this section, the cases in each of the principal wound groups areconsidered separately, and in each of the subdivisions a tabulation lists theimmediate cause of death for the cases in that particular group.

1. The immediate cause of death in the 297 cases in which the principalwound was intracranial is as follows:

	Number of cases		Number of cases
Neural trauma and/or intracranial hemorrhage or clot	210	Pigment nephropathy	2
Shock (all trauma and hemorrhage)	15	Brain abscess	1
Pneumonia	12	Fat embolism (pulmonary)	1
Intracranial blast trauma alone	5	Tracheobronchial obsruction, aspirated vomitus	1
Clostridial myositis, extremity	3	Undetermined, intracranial condition	1
Intracranial blast and other trauma	2	Undetermined, unclassified	40
Thrombotic embolism (pulmonary)	2
Meningitis, intracranial	2

⁴Additional detailed information on surgery,anesthesia, replacement therapy, chemotherapy, oxygen therapy, and othermiscellaneous data are presented in appendix F, p. 813.

500

2. The immediate cause of death in the 27 cases in which the principal woundwas intravertebral is as follows:

	Number of cases
Spinal cord trauma or hematomyelia	16
Shock (all trauma and hemorrhage)	4
Pneumonia	3
Tracheobronchial obstruction, aspirated vomitus	1
Undetermined, unclassified	3

3. The immediate cause of death in the eight cases in which the principalwound was maxillofacial is as follows:

	Number of cases
Tracheobronchial obstruction, blood and mucus	2
Fat embolism (pulmonary)	1
Shock (trauma and hemorrhage)	1
Undetermined, unclassified	4

4. The immediate cause of death in the 25 cases in which the principal woundwas cervical is as follows:

	Number of cases		Number of cases
Shock	¹11	Pigment nephropathy	1
Cerebral ischemia	4	Pneumonia	1
Thrombotic embolism (pulmonary)	2	Tracheobronchial obstruction, blood and mucus	1
Respiratory obstruction (above trachea)	2	Undetermined, unclassified	3

¹Includes 5 cases of cardiorespiratory embarrassment plus trauma andhemorrhage 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:

	Number of cases		Number of cases
Shock	¹70	Clostridial myositis:
Pneumonia	7	Trunk	1
Empyema	5	Extremity	1
Fat embolism (pulmonary)	4	Pulmonary infarction	1
Thrombotic embolism (pulmonary)	3	Mediastinal hemorrhage	1
Cerebral ischemia	3	Myocardial decompensation, general	1
Pigment nephropathy	3	Tracheobronchial obstruction:
Coronary occlusion	2	Aspirated vomitus	1
Anesthetic agent	1	Blood and mucus	1
Pulmonary blast and other trauma	1	Undetermined pulmonary complication	8
Pulmonary blast trauma alone	1	Undetermined, unclassified	23

¹Includes 66 cases of cardiorespiratory embarrassment plus trauma andhemorrhage, 2 cases of contamination or sepsis plus trauma and hemorrhage, and2 cases of trauma and hemorrhage.

6. The immediate cause of death in the 212 cases in which the principal woundwas thoracoabdominal is as follows:

501

	Number of cases		Number of cases
Shock:		Clostridial myositis, trunk	2
Trauma and hemorrhage alone	2	Myocardial decompensation, general	2
Contamination or sepsis plus trauma and hemorrhage	1	Anesthetic agent	1
Contamination or sepsis plus cardiorespiratory embarrassment plus trauma and hemorrhage	59	Pulmonary blast and other trauma	1
	59	Fat embolism (pulmonary)	1
Cardiorespiratory embarrassment plus trauma and hemorrhage	56	Empyema	1
Pigment nephropathy	12	Pulmonary infarction	1
Peritonitis	11	Respiratory obstruction above trachea (maxillofacial wound)	1
Pneumonia	3	Tracheobronchial obstruction, aspirated vomitus	1
Tracheobronchial obstruction, blood and mucus	3	Ventricular arrest	1
Thrombotic embolism (pulmonary)	2	Thoracic trauma, unclassified	1
		Undetermined intracranial complication	1
		Undetermined thoracic complication	3
		Undetermined, unclassified	46

7. The immediate cause of death in the 59 cases in which the principal woundwas combined intra-abdominal and intrathoracic is as follows:

	Number of cases		Number of cases
Shock:		Pigment nephropathy	6
Trauma and hemorrhage alone	4	Fat embolism (pulmonary)	2
Cardiorespiratory embarrassment and trauma and hemorrhage	7	Tracheobronchial obstruction, blood and mucus	2
Cardiorespiratory embarrassment and contamination or sepsis plus trauma and hemorrhage	10	Pulmonary blast trauma alone	1
Contamination or sepsis plus trauma and hemorrhage	4	Air embolism	1
Peritonitis	7	Clostridial myositis, trunk	1
		Neural trauma and/or hemorrhage or clot	1
		Pneumonitis	1
		Undetermined pulmonary condition	1
		Undetermined, unclassified	11

8. The immediate cause of death in the 408 cases in which the principalwound was intra-abdominal is as follows:

	Number of cases		Number of cases
Shock	179	Air embolism	1
Peritonitis	46	Blast trauma alone (pulmonary)	1
Pigment nephropathy	26	Myocardial decompensation (general)	1
Pneumonia	17	Sepsis, abdominal, unclassified	1
Clostridial myositis	9	Septicemia	1
Thrombotic embolism	8	Tracheobronchial obstruction, blood and mucus	1
Tracheobronchial obstruction, aspirated vomitus	5	Transfusion reaction	1
Fat embolism	4	Ventricular arrest	1
Cellulitis, extraperitoneal	3	Other condition (abdominal)	2
Abdominal abscess	2	Undetermined, abdominal cause	4
Anesthetic agent	2	Undetermined, unclassified	91
Intestinal obstruction	2

502

9. The immediate cause of death in the three cases in which the principalwound was of the abdominal wall is as follows:

	Number of cases
Clostridial myositis, trunk	1
Undetermined, thoracic complication	1
Undetermined, unclassified	1

10. The immediate cause of death in the four cases in which the principalwound was upper extremity, soft tissue only, is as follows:

	Number of cases
Shock (trauma and hemorrhage)	1
Pigment nephropathy	1
Undetermined, unclassified	1

11. The immediate cause of death in the 10 cases in which the principal woundwas upper extremity, bone and soft tissue, is as follows:

	Number of cases
Shock (trauma and hemorrhage)	3
Anesthetic agent	1
Clostridial myositis	1
Undetermined, unclassified	5

12. The immediate cause of death in the 31 cases in which the principal woundwas lower extremity, soft tissue only, is as follows:

	Number of cases		Number of cases
Shock (all trauma and hemorrhage)	9	Anesthetic agent	1
Clostridial myositis, extremity	8	Fat embolism (pulmonary)	1
Pigment nephropathy	5	Meningitis, spinal	1
Pneumonia	2	Undetermined, unclassified	4

13. The immediate cause of death in the 114 cases in which the principalwound was unclassified multiple is as follows:

	Number of cases		Number of cases
Shock	46	Cerebral ischemia	1
Fat embolism (pulmonary)	4	Mediastinitis	1
Pigment nephropathy	4	Respiratory failure, cause undetermined	1
Clostridial myositis, extremity	3	Tracheobronchial obstructions:
Intercranial, neural trauma and/or hemorrhage	2	Aspirated vomitus	1
Pneumonia	2	Blood and mucus	1
Abdominal cellulitis	1	Undetermined, unclassified	46
Thrombotic embolism (pulmonary)	4

SPECIAL STUDIES ON INTRA-ABDOMINAL WOUNDS

In 408 cases (28.1 percent) of the 1,450 deaths studied, the principal woundwas intra-abdominal. Adding the 212 cases having thoracoabdominal wounds and the59 cases having combined intra-abdominal and intrathoracic wounds, a total of679 (46.8 percent) deaths were due to wounds of the abdomen. The latter twogroups are not included in the study in this section.

503

The group of 408 cases in which the principal wound was intra-abdominal havebeen studied as a group in the preceding sections of this chapter (p. 501). Inthis section, the 408 cases are considered in further detail.

Shock was the immediate cause of death in 43.6 percent of those 408 deaths inwhich the principal wound was intra-abdominal. An analysis of this group ofshock deaths in abdominal wounds (178 cases) is presented in tables 150 through153 and the tabulations which follow. It was found that 30.9 percent died beforesurgery in this group as compared to 7 percent in the remaining cases (table154). Contamination from a perforated hollow viscus was a factor in 65 percentof those dying from shock (table 151) which was less than the incidence of 74percent in the rest of the group. Hemoperitoneum or continuing hemorrhage wasnoted in 64 percent of the shock group and in 70 percent of the remainder. Therewas very little difference in the incidence of peritonitis in the two groups,the figure approximating 21 percent. Likewise, there was little difference inthe incidence of associated wounds in the two groups (table 152).

In the study of the time interval between wounding to death in the cases withintra-abdominal wounds and dying of shock, it was found that 11 cases lived lessthan 1 hour and 35 cases died before induction of an anesthesia with an averagesurvival time of 16 hours.

TABLE 150.-Datarelative to hospital admission, anesthesia, and surgery in 178 cases in whichthe principal wound was intra-abdominal and the immediate cause of death wasshock

Time of death	Total
Time of death	Number	Percent
Dead on arrival	6	3.4
Dying on admission	11	6.2
Died before anesthesia¹	35	19.6
Died during anesthetic condition	3	1.7
Died during primary surgery	16	9.0
Died subsequent to primary surgery	107	60.1
Total	178	100.0

¹Excludes the DOA and the dying on admission.

The following is a breakdown of the 178 cases in which the principal woundwas intra-abdominal and the immediate cause of death was shock:

	Number of cases		Number of cases
Etiology of shock:		Etiology of shock-Continued
Trauma and hemorrhage	57	Trauma and hemorrhage plus contamination or sepsis plus cardiorespiratory embarrassment	2
Trauma and hemorrhage plus contamination or sepsis	114	Type or etiology undetermined	2
Trauma and hemorrhage plus cardiorespiratory embarrassment	3

504

TABLE 151.-Intra-abdominalpathology in 178 cases¹in which the principal wound was intra-abdominaland the immediate cause of death was shock

Intra-abdominal pathology	Incidence
	Number	Percent
Contamination or sepsis a factor:²
Peritonitis:
Severe	20	10.81
Mild or moderate	17	9.20
Suspected	6	3.24
Primary abdominal hemorrhage	³89	48.11
Recurrent or delayed abdominal hemorrhage	5	2.70
Hemorrhage, profuse in hospital	12	6.49
Total	149	80.55
Contamination or sepsis not a factor:
Peritonitis:
Severe	---	---
Mild or moderate	1	.54
Suspected	---	---
Primary abdominal hemorrhage	³25	13.51
Recurrent or delayed abdominal hemorrhage	4	2.16
Hemorrhage, profuse in hospital	6	3.24
Total	36	19.45
Grand total	185	100.00

¹Contamination or sepsis was a factor in 116 casesand not a factor in the remaining 62 cases.
²Contamination from hollow viscus.
³Includes those cases in which note was made of hemoperitoneum or ofactive intra-abdominal bleeding.

In the 178 cases in which the principal wound was intra-abdominal and theimmediate cause of death was shock, there was an incidence of 193 associatedand, in many instances, multiple wounds, as follows:

	Number of wounds		Number of wounds
Intracranial:		Intrathoracic, suspected	7
Known	1	Upper extremity:
Suspected	5	Bone and soft tissue	9
Scalp	4	Soft tissue only	37
Maxillofacial:		Traumatic amputation	1
Bone and soft tissue	3	Lower extremity:
Soft tissue only	8	Bone and soft tissue	14
Cervical, general	3	Soft tissue only	68
Intraspinal	13	Traumatic amputation	3
Chest wall	17	Total	193
Pulmonary blast injury	1	Total	193

There were no associated wounds in 60 of these 178 cases.

505

FIGURE 263.-Plasmabeing administered to a casualty at a battalion aid station.

The records of plasma and blood administered can be verydifficult to interpret. In a surprisingly large percentage of cases, there wasno record of any blood transfusion. It is possible that some received blood andno record was made, but also probable that in the majority no blood wasadministered. The averages given (table 152) are based only on those cases inwhich blood was given and a record made of its administration. The data on theamount of plasma administered before admission represent the replacement therapycarried out in battalion aid stations (fig. 263), collecting stations, andclearing stations. While it is believed that only the minimum amount of plasmanecessary to insure transportability of the patient should be given, just whatthat amount is in each case has to be determined by the individual medicalofficer in charge. That his judgment had been excellent in nearly every case isa statement to which medical officers in Army hospitals will attest. Comparingthe averages and the number receiving blood in the group dying in shock with thewhole group of cases, it was found that a larger percentage of cases received alarger 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 handfor the cases with intra-abdominal wounds who lived, comparisons could not bemade with a group of cases in which therapy was adequate.⁵

⁵It is our opinion that in the group of cases who died the amount of blood administered was inadequate.-H. E. S. and J. W. C.

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TABLE 152.-Transfusionrecord in group of 178 cases in which the principal wound was intra-abdominaland the immediate cause of death was shock

Time of transfusion	Number receiving transfusion of-		Average number of units administered
Time of transfusion	Plasma	Blood	Plasma (250 cc. units)	Blood (500 cc. units)
Before admission	130	---	3.18	---
After admission, before surgery	77	112	3.16	3.03
During surgery	23	55	2.95	3.19
After surgery	16	27	2.25	3.07

The percent of bullet wounds in the shock deaths in the intra-abdominal groupwas 17.4 percent (table 153) as compared with 19.6 percent in the entireintra-abdominal group, while in the whole series (1,450) it was only 15.0percent.

TABLE 153.-Distributionof group of 178 cases in which the principal wound¹was intra-abdominal and the immediate cause of death was shock, by causativeagent

Causative agent	Number of cases	Percent of cases
Bullet:
Unclassified	23	12.9
Rifle	2	1.1
Machinegun	6	3.4
High explosive:
Unclassified	17	9.5
Shell	116	65.2
Mine	3	1.7
Boobytrap	---	---
Bomb	8	4.5
Blast	---	---
No record	3	1.7
Total	178	100.0

¹The type of wound in this group was penetrating in125 cases and perforating in 53 cases.

The following tabulation lists the miscellaneous conditions occurring in thegroup of 178 cases with intra-abdominal wounds who died of shock:

	Number of cases		Number of cases
Myocardial decompensation:		Tracheobronchial obstruction-Con.
Evident	2	Blood and mucus	3
Suspected	14	Suspected	1
Pulmonary edema:		Thoracic trauma (chest wall)	18
Severe	1	Pigment nephropathy:
Slight or moderate	12	Evident	1
Tracheobronchial obstruction:		Suspected	5
Aspirated vomitus	---	Renal trauma, evident	24

507

Myocardial decompensation was evident in only two cases, and, in these,excessive administration of plasma and blood was thought responsible. Pulmonaryedema was noted in 13 cases in the group. As this is an unusual occurrence inuncomplicated shock, a search was made for factors predisposing to pulmonaryedema. All 13 cases received plasma and blood before surgery. The average unitsreceived were little different from the averages for those receiving plasma andblood in the rest of the group in which, however, a substantial number receivednone. It was difficult to draw any conclusions regarding the role plasma andblood played in the appearance of pulmonary edema in this group. Thoracictrauma, blast trauma, and pneumonia probably contributed to the incidence of"pulmonary edema."

Study of blood pressure records revealed that 17 of the 55 recorded admissionblood pressures were zero. The lowest pressure recorded was zero in 34 of the 70cases where records were available. The average duration of surgery in thisshock group approached 2? hours. All cases coming to surgery received etheranesthesia. Thiopental sodium (Pentothal sodium) was used once and nitrous oxide40 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 ofdeath was not shock. It should be noted that there was no evidence of shock inonly six of these cases. The remainder had evidence of shock at some time duringthe course of their hospital stay.⁶ Analysis ofshock as a contributory or associated condition is included in the study of thisgroup of cases.

The incidence of shock as a contributory or associated condition in the groupof 230 cases in which the principal wound was intra-abdominal and the immediatecause of death was not shock follows:

Contributory or associated condition of shock:	Number of cases
Corrected by therapy	121
Suspected, not proved	16
Present, successful correction doubtful	66
Uncorrected	21
No evidence	6

⁶The terminal fall in blood pressure occurring in every case immediately before death was not regarded as evidence of shock.

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TABLE 154.-Datarelative to hospital admission, anesthesia, and surgery, in 230 cases in whichthe principal wound was intra-abdominal and the immediate cause of deathwas not shock

Time of death	Number of cases	Percent of cases
Dead on arrival	---	---
Dying on admission	1	0.4
Died before anesthesia¹	10	4.4
Died during anesthetic induction	5	2.2
Died during primary surgery	4	1.7
Died subsequent to primary surgery	210	91.3
Total	230	100.0

¹Excludes the DOA and those dying on admission.

Miscellaneous findings in 230 cases in which the principal wound wasintra-abdominal but the immediate cause of death was not shock but with shock asa contributory or associated condition (224 cases) were as follows:

Hemorrhage:	Number of cases
Profuse in hospital	11
Primary	156
Recurrent or delayed	10
Peritoneal contamination from hollow viscus	165
Peritonitis:
Severe	17
Mild or moderate	31
Suspected	40

In the 230 cases in which the principal wound was intra-abdominal but theimmediate cause of death was not shock, the incidence of associated wounds wasas follows:

	Number of cases		Number of cases
Associated wounds:		Associated wounds-Continued
Intracranial:		Pulmonary blast	4
Known	1	Intrathoracic, suspected	10
Suspected	1	Thoracoabdominal	1
Scalp	3	Upper extremity:
Maxillofacial, bone and soft tissue	1	Soft tissue only	28
Eye or orbit	2	Traumatic amputation	1
Maxillofacial and soft tissue only	7	Lower extremity:
Neck, general	6	Soft tissue only	72
Intraspinal, unclassified	13	Bone and soft tissue	46
Chest wall only	22	Traumatic amputation	2

There were no associated wounds in 70 of the 230 cases.

A further breakdown of the group of 408 cases in which the principal woundwas intra-abdominal is presented in tables 155 through 159. The data presentedin those tables are for a group of 175 cases in which peritonitis was

509

evident or suspected to be present. It was believed that a better picture ofintra-abdominal wounds might be obtained if they were not complicated by factorsoriginating from concomitant wounds of the chest and diaphragm. Those withperitonitis and suspected peritonitis were examined in three groups (table 155).The first group was composed of those in which peritonitis was the immediatecause of death. In the second group, peritonitis was evident but not theimmediate cause of death. This included the cases listed under contributory orassociated conditions as "peritonitis, severe" and "peritonitis,mild or moderate." The third group was made up of those cases in whichperitonitis was suspected but the evidence was not sufficient to confirm itspresence.

TABLE 155.-Data relativeto hospital admission, anesthesia, and surgery, in 175 cases in which theprincipal wound was intra-abdominal and peritonitis was evident or suspected tobe present

Time of death	Peritonitis immediate cause of death	Peritonitis contributory to death	Peritonitis suspected
Before anesthesia	---	2	---
During anesthetic induction	---	2	---
During primary surgery	---	3	---
After primary surgery	46	76	46
Total	46	83	46

TABLE 156.-Operatingtime for primary surgery in 175 cases in which the principal wound wasintra-abdominal and peritonitis was evident or suspected to be present

Operating time (minutes)	Peritonitis immediate cause of death	Peritonitis contributory to death	Peritonitis suspected
Less than 30	---	2	---
30 to 59	---	1	---
60 to 89	1	---	1
90 to 119	1	3	1
120 to 149	---	5	3
150 to 179	3	4	---
180 to 209	4	6	---
210 to 239	2	1	---
240 to 299	1	1	---
300 to 360	---	1	---
Not stated	34	59	41
Total	46	83	46
Average time	180	154	117

510

TABLE 157.-Datarelative to primary surgery on 175 cases in which the principal wound wasintra-abdominal and peritonitis was evident or suspected to be present

Type of surgery	Peritonitis immediate cause of death		Peritonitis contributory to death		Peritonitis suspected		Total
Type of surgery	Number	Percent of operations	Number	Percent of operations	Number	Percent of operations	Number	Percent of operations
Laparotomy	45	49.4	80	49.1	44	48.9	169	.1 49
Debridement, abdominal wall wound only	---	---	2	1.2	1	1.1	3	.9
Debridement, other wounds:
Associated with primary operation	41	45.1	44	27.0	26	28.9	111	32.3
Omitted deliberately	1	1.1	4	2.5	1	1.1	6	1.7
Partially done	1	1.1	8	4.9	---	---	9	2.6
Not stated	3	3.3	25	15.3	18	20.0	46	13.4
Total	91	100.0	163	100.0	90	100.0	344	100.0

TABLE 158.-Theimmediate cause of death in 175 cases in which the principal wound wasintra-abdominaland peritonitis was evident or suspected to be present

Immediate cause of death	Peritonitis immediate cause of death	Peritonitis contributory	Peritonitis suspected
Peritonitis	46	---	---
Shock	---	39	6
Pigment nephropathy	---	12	---
Pneumonia	---	9	2
Fat embolism (pulmonary)	---	3	---
Thrombotic emobolism (pulmonary)	---	2	---
Cellulitis, abdominal	---	1	1
Clostridial myositis:
Trunk	---	1	---
Extremity	---	1	1
Intestinal obstruction	---	1	---
Sepsis, abdominal, unclassified	---	1	---
Tracheobronchial obstruction, aspirated vomitus	---	1	---
Transfusion reaction	---	---	1
Undetermined:
Abdominal	---	2	---
Unclassified	---	14	35
Total	46	87	46

511

TABLE 159.-Etiology ofshock as a contributory or associated condition in 175 cases in which theprincipal wound was intra-abdominal and peritonitis was evident or suspected tobe present

Etiology or type of shock	Peritonitis immediate cause of death	Peritonitis contributory	Peritonitis suspected
Cardiorespiratory embarrassment plus trauma and hemorrhage	1	---	1
Cardiorespiratory embarrassment plus trauma and hemorrhage plus contamination or sepsis	---	1	---
Contamination of sepsis plus trauma and hemorrhage	42	41	35
Trauma and hemorrhage	1	6	4

CASES IN WHICH THE IMMEDIATE CAUSE OF DEATH WAS SHOCK

The 523 cases which have been listed under this heading werethose in which there was good evidence of peripheral circulatory failureinitiated by the initial trauma and hemorrhage and perpetuated by trauma andhemorrhage with or without the added shock-producing factors ofcardiorespiratory embarrassment, peritoneal contamination from a wound of ahollow viscus or early sepsis, or any combination of these factors. The data onthe "Etiology of shock" reveal the evidence of these various factors.No effort was made to separate the factors of trauma and hemorrhage, as bothoccurred in varying degrees and proportions in every battle casualty. In 13cases, recurrent or delayed abdominal hemorrhage was a factor. In the 245 caseswho died of shock after primary surgery, only 43 lived more than 24 hours afterthe surgery.

Tables 160 through 165 which follow relate to the 523 casesin the series of 1,450 deaths in which shock was listed as the immediate causeof death. In addition, there were 750 other cases in which shock was acontributory or associated condition. There was no evidence of shock in only 177of the 1,450 deaths studied. It is not within the province of this report todiscuss in detail the etiology of shock. However, it should be stated thatclinical experience and laboratory investigations demonstrated that loss ofwhole blood was the most important factor in the vast majority of battlecasualties in shock. The amount of blood lost was far in excess of previousestimates. In 1945, whole blood was given to 40.6 percent of the battlecasualties admitted to Fifth U.S. Army hospitals at a rate of 2.52 pints percasualty transfused.⁷ Many casualties weregiven as much as 6 or 8 pints of blood and a few even more in the first 24 hoursafter their admission to the hospital. Plasma loss per se was found only inburns, crush injuries, gas gangrene, sepsis, and gross

⁷Data based on reports of hospitals to the Fifth U.S. Army surgeon.

512

contamination of the peritoneal or pleural cavities.⁸In the latter two categories, plasma loss was often less than whole bloodloss. Inasmuch as blood was not available except in exceptional circumstances atbattalion aid and collecting and clearing stations, some of the most severelywounded casualties, or those in the most severe grade of shock from theirwounds, were often given large quantities of plasma to render them transportableto the hospital. These casualties were frequently again in severe shock by thetime they arrived at the hospital, and further resuscitation was complicatedbecause the remaining blood in their vascular tree was well diluted with plasma.

Among contributing factors in shock deaths were thefollowing:

1. The use of large quantities of plasma to combat loweredblood volume when the loss has been of whole blood.

2. Unrecognized and/or uncontrolled continued bleeding.

3. Inadequate or poorly timed blood replacement with wholeblood.

4. Delayed surgery in those cases in which there has beengross contamination of peritoneal and pleural cavities with contents of thegastrointestinal tract, or in which sepsis is developing.

TABLE 160.-Location ofprincipal wound in 523 cases in which the immediate cause of death was shock

Location of principal wound	Number of cases	Percent of cases
Intra-abdominal	178	34.03
Thoracoabdominal	118	22.56
Intrathoracic	70	13.39
Unclassified, multiple	46	8.80
Lower extremity, bone and soft tissue	41	7.84
Combined intra-abdominal and intrathoracic	25	4.78
Intracranial	15	2.87
Cervical	11	2.10
Lower extremity, soft tissue	9	1.72
Intravertebral	4	.77
Upper extremity:
Bone and soft tissue	3	.57
Soft tissue	2	.38
Maxillofacial	1	.19
Abdominal wall	---	---
Total	523	100.0

⁸(1) Stewart, J. D., and Warner, F. F.: Observations on the Wounded in Forward Field Hospitals With Special Reference to Wound Shock. Ann. Surg. 122: 129, 1945. (2) Simeone, F. A.: Personal communication to the authors based on work of the Board for the Study of the Severely Wounded.

513

5. Failure to recognize and/or control factors leading to cardiorespiratoryembarrassment. Included in this group are hemothorax, pneumothorax, cardiactamponade, tracheobronchial obstruction from blood or mucus, painful chest wallwounds, and gastric dilatation.

6. Failure to control pain by morphine, procaine hydrochloride (Novocain)nerve block, proper splinting of painful extremity wounds, and timely surgery.

TABLE 161.-Datarelative to hospital admission, anesthesia, and surgery in 523 cases in whichthe immediate cause of death was shock

Time of death	Number of cases	Percent of cases
Dead on arrival	25	4.8
Dying on admission	55	10.5
Died before anesthesia¹	135	25.8
Died during anesthetic induction	6	1.1
Died during primary surgery	48	9.2
Died subsequent to primary surgery	254	48.6
Total	523	100.0

¹Excludes the DOA and those dying on admission.

TABLE 162.-Etiology ofshock in 523 cases in which shock was the immediate cause of death

Etiology of shock	Number of cases in group-						Total number of cases
Etiology of shock	I	II	III	IV	V	VI	Total number of cases
Trauma and hemorrhage	15	35	71	---	10	53	184
Contamination or sepsis plus trauma and hemorrhage	1	2	10	3	11	93	120
Cardiorespiratory embarrassment plus trauma and hemorrhage plus contamination or sepsis	1	1	10	---	12	48	72
Cardiorespiratory embarrassment plus trauma and hemorrhage	8	17	44	3	15	60	147
Total	25	55	135	6	48	254	523

NOTE.-Key for roman numerals:
I Dead on arrival.
II Dying on admission.
III Died before anesthesia (excludes I andII).
IV Died during anesthetic induction.
V Died during primary surgery.
VI Died subsequent to primary surgery.

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TABLE 163.-Lowestrecorded blood pressure¹and other evidence in 498 cases in which the immediatecause of death was shock

Blood pressure record and evidence of shock	Number of cases in group-					Total number of cases
Blood pressure record and evidence of shock	II	III	IV	V	VI	Total number of cases
Shock present:
0	10	26	1	7	47	91
2 to 38	---	---	1	1	2	4
40 to 58	---	10	---	2	16	28
60 to 78	1	9	1	3	28	42
80 to 88	2	7	---	2	18	29
90 to 98	---	3	---	2	8	13
100 or more, but pulse rapid and weak²	---	---	---	1	3	4
Presence of shock recorded	18	52	2	15	77	164
Shock suspected by inference	9	7	---	2	4	22
Treatment suggests shock	15	21	1	13	51	101

¹Excluding the gradual terminaldecline immediately preceding death.
²No comment on shock in record.

NOTE.-Key for roman numerals:
II Dying on admission.
III Died before anesthesia (excludesII).
IV Died during anesthetic induction.
V Died during primary surgery.
VI Died subsequent to primarysurgery.

TABLE 164.-Primaryoperations performed on 327 cases in which the immediate cause of deathwas shock

Type of operation	Died during primary surgery	Died following primary surgery	Total number of cases
Abdominal stab incision	1	6	7
Amputation	2	17	19
Craniotomy	1	4	5
Debridement only	5	36	41
Laminectomy	1	3	4
Laparotomy	5	168	173
Other operation	1	3	4
Thoracolaparotomy	3	7	10
Thoracotomy	14	50	64

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TABLE 165.-Miscellaneousobservations in 219 cases in which the immediate cause of death was shock

Miscellaneous observations	Number of cases in group-					Total number of cases
Miscellaneous observations	II	III	IV	V	VI	Total number of cases
Burns present	2	3	---	---	4	9
Coma on admission	8	20	---	1	7	36
Cyanosis, marked	---	2	---	3	4	9
Dying on admission	55	---	---	---	---	55
Exposure, severe, before admission	---	---	---	---	2	2
Hemorrhage, profuse, in hospital	---	1	---	9	19	29
Pallor noted	4	2	---	1	2	9
Peritoneal closure impossible	---	---	---	---	4	4
Sweating noted	1	2	---	---	2	5
Tourniquet used before admission	6	10	---	1	12	29
Two or more of these present	18	6	---	1	7	32

NOTE-Key for roman numerals:
II Dying on admission.
III Died before anesthesia (excludes II).
IV Died during anesthetic induction.
V Died during primary surgery.
VI Died subsequent to primary surgery.

PIGMENT NEPHROPATHY IN BATTLE CASUALTIES

The development of progressive oliguria and anuria in battlecasualties resuscitated from shock and apparently on the road to recoveryfollowing extensive surgical procedures led to the death of a significant numberof severely wounded soldiers. Death usually occurred between the fourth andeighth days after the wound was incurred. At autopsy, the kidneys were observedto be somewhat enlarged, and on microscopic examination pigment casts were seenin the distal convoluted and collecting tubules. The proximal tubules weredilated, and a varying degree of necrosis of the distal tubules was observed,with some inflammatory reaction in the adjacent stroma. The capillary tufts inthe glomeruli showed no changes, but there was in some cases slight swelling ofthe cells in Bowman's capsule. This lesion has been variously termed pigmentnephropathy, hemoglobinuric nephrosis, and lower nephron nephrosis.

Among the 1,411 deaths, lower nephron nephrosis or pigmentnephropathy led to death in 68 cases (table 166) and contributed to death in 31others. It was suspected to have been present in 57 additional cases. Autopsywas performed in all but 9 of the 99 cases in which pigment nephropathy wasknown to be present, and microscopic study of renal sections was reported in 67of the 90 cases in which autopsy was performed.

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TABLE 166.-Distributionof 1,411 hospital battle casualty deaths, by result or status of pigment nephropathy

Result or status of pigment nephropathy	Number of cases	Percent of cases
Led to death	68	4.8
Contributed to death	31	2.2
Suspected	57	4
Total	156	11

A study of the 99 cases in which pigment nephropathy wasknown to be present forms the basis of this presentation. Of significance arethe severity and multiplicity of wounds encountered in this group. The followingtabulations list the site of the principal wounds and of the associated woundsin this group of 99 cases of pigment nephropathy:

Site of principal wounds:	Number of cases	Site of principal wounds-Con.	Number of cases
Intra-abdominal area	45	Lower extremity	18
Combined intra-abdominal and intrathoracic area	6	Upper extremity	1
Thoracoabdominal area	8	Cervical area	2
Intrathoracic area	4	Unclassified, multiple areas	5
Intracranial area	8	Total	99
Intraspinal area	2	Total	99
Site of associated wounds:	Number of wounds	Site of associated wounds-Con.	Number of wounds
Intracranial area	5	Combined intra-abdominal and intrathoracic area	1
Maxillofacial area (bones and soft tissue)	3	Intra-abdominal area	1
Eye or orbit	3	Suspected intra-abdominal area	3
Maxillofacial area (soft tissue only)	9	Upper extremity (includes 2 traumatic amputations)	44
Neck	9	Lower extremity (includes 2 traumatic amputations)	49
Intraspinal area	7	Total	149
Thoracic wall	6
Intrathoracic area	10
Suspected intrathoracic area	2
Abdominal wall (exclusive of intra-abdominal cases)	7

It will be noted that the abdominal cavity was involved in 59cases and that intra-abdominal wounds were present as associated wounds in 2more cases and suspected in 3 others. In only 20 cases were no wounds presentother than the one or ones listed as principal wounds. The 149 associated woundsoccurred in 79 cases, for a total of 238 wounds.⁹

⁹Multiple wounds confined to one region of the body, such as the lower extremity or the intra-abdominal area, were listed as only one wound. The same is true of the 20 cases in which no associated wounds are listed, as in many of these cases there were multiple shell fragment or bullet wounds confined to one region of the body.

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In all the deaths in battle casualties studied, attempt wasmade to ascertain an immediate cause of death. Lower nephron nephrosis wasregarded as the immediate cause of death in 68 cases. In 31 cases, some othercause was thought to be the immediate cause of death, as is shown in thefollowing tabulation:

Immediate cause of death	Number of cases	Immediate cause of death-Con.	Number of cases
Fat embolism	3	Pneumonia	2
Thrombotic pulmonary embolism	3	Shock	5
Clostridial myositis (gas gangrene)	4	Spinal cord trauma	1
Intracranial hemorrhage, trauma	3	Undetermined intra-abdominal lesion	2
Peritonitis	1	Unclassified, undetermined	7

The so-called immediate cause of death, however, fails to give a completepicture of the multiplicity of pathologic conditions existing in this group of99 cases. The contributory or associated conditions existing in this group areshown in the tabulation which follows:

TABLE

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Pulmonary complications were so frequent as to be almost the rule. In manycases, the giving of intravenous fluids in the absence of urinary excretion ledto high volume of the blood, cardiac failure, and pulmonary edema. Toxic hepaticdegeneration was present in 16 cases, epidemic hepatitis in 4 cases (suspectedin 1 more), and septic hepatitis secondary to trauma in 2 cases (suspected in 3more). There was recorded evidence of renal trauma in 18 of the 99 cases, and aureter had been traumatized or tied in 3 other cases. Fat embolism was theimmediate cause of death in 3 cases, contributing cause of death in 8 cases, andwas suspected as contributory to death in 4 more cases. The 11 cases in 99represent an incidence of 11 percent, which is considerably higher than in thewhole series of 1,411 battle casualty deaths, in which 49 cases constitute only3.5 percent. It is also interesting to note that, in the 49 patients known tohave pulmonary fat embolism, 11 had pigment nephropathy. Severe reactions fromblood transfusion were noted in only 3 of the 99 cases. Gross infection wasevident in 61 cases.

One outstanding feature in the cases in which anuria developed was theseverity of the shock which occurred sometime between wounding and thedevelopment of renal insufficiency. In the 99 cases in which pigment nephropathywas known to exist, the lowest recorded blood pressures, along with other datarelative to shock, are as follows:

	Number of cases
Systolic blood pressure recording:
0	22
2-38	1
40-58	9
60-78	13
80-88	6
90-98	5
Presence of shock stated (no other data)	13
Treatment suggests shock (no other data)	25
No evidence of shock	5
Total	99

The five cases, the records of which gave no evidence of shock, are ofsufficient 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. Dataregarding the duration of low blood pressure were available in only a fewinstances. No data concerning the level of blood pressure before admission to ahospital are available. The amount of plasma administered before admission isperhaps the best index of shock at that time. The number of

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units of 250 cc. of plasma administered in 99 cases of pigment nephropathybefore admission to a hospital installation was as follows:

Units of plasma:	Number of cases	Units of plasma-Continued	Number of cases
None or no record	25	5	3
1	16	6	1
2	19	8	1
3	22	10	1
4	10	11	1

There was evidence of shock in 94 of the 99 cases of pigmentnephropathy. Trauma and hemorrhage were the leading causative factors in thedevelopment of shock. Additional contributory factors were cardiorespiratoryembarrassment and contamination of the peritoneum or of an extremity. Theamounts of plasma and blood used after admission to the hospital are furtherindexes of the degree of shock in these patients. The recorded data availableconcerning the administration of plasma and of blood are shown in the followingtabulation:

Units of plasma administered-	Number of cases	Units of plasma administered-Con.	Number of cases
Before admission:		During operation-Con.
No record	25	7	---
1	16	8	---
2	19	9	---
3	22	10	---
4	10	11	---
5	3	After operation:
6	1	No record	68
7	---	1	7
8	1	2	7
9	---	3	5
10	1	4	5
11	1	5	---
After admission, before operation:		6	4
No record	60	7	2
1	12	8	1
2	16	9	---
3	4	10	---
4	2	11	---
5	2	Pints of blood administered-
6	2	Before operation:
7	---	No record	33
8	---	1	10
9	---	2	10
10	---	3	13
11	1	4	14
During operation:		5	11
No record	75	6	3
1	9	7	2
2	8	8	1
3	2	9	2
4	2	10	---
5	1	11	---
6	2

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Pints of blood administered-Con.	Number of cases	Pints of blood administered-Con.	Number of cases
During operation:		After operation:
No record	45	No record	49
1	14	1	23
2	14	2	8
3	6	3	5
4	6	4	8
5	2	5	4
6	5	6	1
7	2	7	1
8	2	8	---
9	2	9	---
10	---	10	---
11	1	11	---

Treatment with oxygen might be expected in a larger percentage of patientsthan is shown in the following tabulation:

Oxygen therapy:	Number of cases	Oxygen therapy-Continued	Number of cases
No record	36	During operation	47
Before operation	13	After operation	27

The operating time for primary surgical treatment, shown in the tabulationwhich follows, is a further index of the severity of the wounds in this group ofcases.

Operating time (minutes):	Number of cases	Operating time (minutes)-Con.	Number of cases
Less than 30	---	180-209	7
30-59	---	210-239	2
60-89	1	240-299	4
90-119	3	300-359	2
120-149	2	More than 360	2
150-179	3

Unfortunately, the time was not stated in 62 of the cases; nooperation was performed in 11 cases. In the remaining 26 cases, however, it wasseen that in only one case did the operation last less than 1? hours, while inthe largest group of cases the operating time was from 3 to 3? hours.

Data concerning anesthesia in the 68 patients who died ofpigment nephropathy are presented in table 167. It will be noted that, with theexception of four patients who died before anesthesia was complete, all of whomhad crush injuries, all had been given ether. In table 168, the anesthesia in 31cases in which pigment nephropathy was a contributing cause of death isrecorded. Of this group, seven patients died before anesthesia was complete; onehad local anesthesia only; and all of the rest had ether anesthesia in one formor another. The patient who had local anesthesia only had an intracranial woundand died of pneumonia, septic hepatitis, and jaundice. There was a record ofadequate urinary output and no evidence of shock. On the basis of microscopicautopsy alone, the diagnosis of pigment nephropathy was made. Data for sevenpatients who died before the induction of anesthesia

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in this group are presented in table 169. The diagnosis ofpigment nephropathy in each of these cases is based on microscopic study ofrenal sections. All the patients had severe wounds; most of them died after acomparatively short time of being wounded, and correction of shock was doubtfulor shock was completely uncorrected in all but one patient. Data concerning theamount of urine passed were unavailable. Since ether was considered to be theanesthetic of choice in all battle casualties with shock or severe wounds, nosignificance can be attached to the high incidence of ether anesthesia in thisgroup of patients with pigment nephropathy.

TABLE 167.-Anesthesiain 68 patients who died of pigment nephropathy

Type of anesthesia	Number of patients at-
	Primary operation	Secondary operation
Ether:
Closed system	31	2
Open drop	3	0
Unclassified	15	2
Endotracheal¹	28	1
Nitrous oxide¹	28	2
Thiopental sodium¹	3	2
No record	14	3
Death occurred before induction of anesthesia²	4	3

¹All were known to have had ether, alone or incombination with another agent.
²All had crush injuries.

TABLE 168.-Anesthesiain 31 patients in which pigment nephropathy contributed to death

Type of anesthesia	Number of patients at-
	Primary operation	Secondary operation
Ether:
Closed system	13	1
Flagg method	1	4
Open drop	1	0
Unclassified	5	0
Endotracheal	7	0
Nitrous oxide	11	1
Local¹	1	1
Thiopental sodium	0	0
No record	3	2
Death occurred before anesthesia was complete	7	0

¹Specific agent not known.

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TABLE 169.-Analysis of7 cases in which death occurred before anesthesia and in which pigmentnephropathy contributed to death¹

Wounds	Immediate cause of death	Shock	Timelag from wounding to death (hours)	Urinary output
Intracranial and the abdominal wall.	Pulmonary embolism (thrombotic).	Uncorrected; lowest blood pressure recorded 60/20.	Not recorded.	Recorded inadequate.
Intraspinal, neck, intrathoracic (bilateral), and upper extremity.	Undetermined	Corrected; administered blood; pressure 50/0.	14	No record.
Intracranial (bilateral) and multiple.	Shock	Uncorrected	33	Do.
Intraspinal, intracranial, maxillofacial, neck, and upper extremity.	Spinal cord trauma.	Shock; correction doubtful	113	Do.
Traumatic amputation and lower extremity.	Fat embolism.	...do...	25	Do.
Multiple, extremities, and face.	Gas gangrene.	Uncorrected	76	Record inadequate.
Intracranial, both lower extremities, and one upper extremity.	...do...	...do...	73

¹Diagnosis of pigment nephropathyin each instance was based on microscopic study of renal sections.

When the first cases of anuria were encountered, thesulfonamide drugs were regarded as the probable causative factor. Sulfanilamidepowder was dusted into almost every wound on the battlefield, and most of thewounded soldiers had taken 4 gm. by mouth before reaching the hospital. Early inthe period under study, it was common practice to administer 5 gm. of asulfonamide drug intravenously to all with abdominal wounds immediately onadmission to the hospital and to repeat this dose at intervals of 12 to 24 hoursthereafter. With the appearance of anuria, this practice was discontinued, andno sulfonamide drug was given intravenously until 12 hours after operation andonly after the patient had fully reacted from shock. At the same time, theamount 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

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a causative factor at least in one case, cannot be refuted. That they werenot the only factor except in a few cases, likewise, was evident from subsequentstudies. In 30 of the 68 cases in which pigment nephropathy was the direct causeof death and in 14 of the 31 cases in which pigment nephropathy contributed todeath, there was no record of sulfonamide therapy, excluding the sulfanilamidepowder dusted into wounds at the time of the first aid dressing.

The microscopic observation of a lesion termed hemoglobinuric nephropathyfocused attention on blood transfusion as a causative factor. Before theestablishment of a blood bank unit in the Mediterranean theater, reactions frommismatched 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 togroup A or group B recipients might be responsible for anuria in some of thecases; however, low titer group O blood (containing anti-A and anti-B isoagglutinins in a titer of less than 1 to 120) was used for all except group Orecipients, and it was later ascertained¹⁰that the incidence of pigment nephropathy in the persons of the four bloodgroups paralleled the relative incidence for persons of the four groups in thegeneral population. In a separate article,¹¹ acase of Maj. James M. Mason's was mentioned in which a group A recipientreceived 5,500 cc. of low titer group O blood before and during operation for athoracoabdominal wound, which involved the removal of one kidney. There was noevidence of insufficiency in the remaining kidney, and the patient made anuneventful recovery. It was likewise demonstrated¹²that the shock occurring in battle casualties was due in most instances to lossof whole blood and that the apparently massive doses of blood used inresuscitation of these patients were excessive in only a few instances. In mostcases, determinations of the volume of blood established the fact that notenough whole blood was being used in the resuscitation of these patients. It wasalso observed that many patients showing gross hemoglobinuria did not alwaysexperience renal insufficiency, while, on the other hand, in many of the fatalcases of pigment nephropathy hemoglobinuria was never apparent grossly.

Early in 1944, at the same time that a reduction in the use of sulfonamidedrugs was effected, the use of sodium bicarbonate to render the urine alkalinewas encouraged. In many cases, it was given by mouth as soon as treatment withsulfonamide drugs was started; in others, it was given intravenously beforesulfonamide medication and blood transfusion. Records regarding this treatmentwere seldom complete, but in the 99 cases of nephropathy the use of sodiumbicarbonate was reported in 21 cases.

¹⁰Mallory, T. B.: Hemoglobinuric Nephrosis in Traumatic Shock, Am. J. Clin. Path. 17:427-443, June 1947.
¹¹Snyder, H. E., and Culbertson, J. W.: Causes of Death in Battle Casualties Reaching Hospitals. Am. J. Surg. 73:184-198, February 1947.
¹²(1) Report, J. J. Lalich, to Commanding Officer, 2d Auxiliary Surgical Group, June 1944, subject: Transfusion Therapy in the Battle Casualty Exhibiting Evidence of Circulatory Failure. (2) Report, J. J. Lalich, to Surgeon, Mediterranean Theater of Operations, U.S. Army, November 1944, subject: Hematocrit and Plasma Protein Findings in Battle Casualties Treated in a Field Hospital.

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The hepatorenal syndrome was considered as a mechanism which might accountfor anuria in some of the cases. The reports of Orr, Helwig, and Schutz¹³constituted the chief source of information for American surgeonsconcerning renal shutdown associated with trauma. It was apparent, however, thatthe majority of patients seen did not present evidence of hepatic damage,although such damage was present in no inconsiderable percentage. Review of themicroscopic renal observations in the cases reported by Orr and Helwig wouldlead one to believe that the condition they described was pigment nephropathy.

Luck?¹⁴ reviewed 538 cases in which thedisease was fatal, the records and material of which were received at the ArmyInstitute of Pathology during the war. He found the characteristic renal lesionin 11 groups, which included cases in which there were battle wounds, crushinginjuries, abdominal operations, burns, reactions from blood transfusion,intoxication due to sulfonamide drugs, heat prostration, malaria due toinfection with Plasmodium falciparum (black-water fever), poisoning dueto a variety of agents, hemolytic anemia, edema, and such unrelated conditionsas uteroplacental damage, acute pancreatitis, and rickettsial disease.

With increasing experience with the condition, it became the opinion of manythat the severe degree of shock occurring in most of the cases must beresponsible at least in part for the development of nephrosis. In the fall of1944, a board¹⁵for the study of theseverely wounded was appointed by Col. Edward D. Churchill, MC, Consultant inSurgery, Mediterranean theater. This board made elaborate studies, both clinicaland laboratory, on battle casualties in severe shock¹⁶when admitted to forward hospital installations and all observations ofpractical value were made available immediately in the forward hospitals. Beforethis time, clinical observation by many and laboratory investigation by Stewart,Lalich, and others had led to the general belief that shock in persons sufferinginjury in battle was in most cases due to loss of whole blood. The studies ofthe board confirmed this opinion and defined the exceptions to the rule. It waslearned that in the cases in which nephropathy developed the observation of abenzidine-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 casesof crush injury but that in the other cases it might be hemoglobin or myoglobinor a combination thereof. Except in the cases in which there were crushinjuries, it was impossible to predict from the nature of the injury what typeof pigment would be seen in the urine. Mallory, a member of the board, observedthat it was not possible by micro-

¹³(1) Orr, T. G., and Helwig, F. D.: Liver Trauma and the Hepatorenal Syndrome. Ann. Surg. 110:682-692, October 1939. (2) Helwig, F. D., and Schutz, C. B.: A Liver Kidney Syndrome. Surg., Gynec. & Obst. 55:570-580, November 1932.
¹⁴Luck?, B.: Lower Nephron Nephrosis. Mil. Surgeon 99:371-396, November 1946.
¹⁵Members of the Board for the Study of the Severely Wounded were as follows: Lt. Col. Henry K. Beecher, MC, Lt. Col. Fiorindo A. Simeone, MC, Lt. Col. Tracy B. Mallory, MC, Maj. Eugene R. Sullivan, MC, Capt. Charles H. Burnett, MC. Capt. Louis D. Smith, SnC, and Capt. Seymour L. Shapiro, SnC.
¹⁶Medical Department, United States Army. Surgery in World War II. The Physiologic Effects of Wounds. Washington: U.S. Government Printing Office, 1952.

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scopic study of the kidneys to determine whether a lesion had been producedby poisoning due to sulfonamide drugs, mismatched transfused blood, or otherfactors. Mallory pointed out that the deposit of pigment in the distalconvoluted and collecting tubules does not seem to be the first pathologicchange in the kidneys. In 11 of their patients who died of injury within 72hours, only 2 showed pigment casts in significant numbers.

Before the appearance of pigment casts, a fine fat vacuolization of ascendinglimbs of Henle's loops appears. Mallory stated that this appears in 75 or 80percent of patients who experienced shock, regardless of whether clinicalevidence of renal insufficiency develops or not, and that the process isreversible. He expressed the belief that the pigment casts play no role in theinitiation of renal insufficiency following shock but that one cannot state thatthey have no effect in the later stages of the disease. The dilatation of therenal tubules proximal to the casts and about them would lead to the assumptionthat they do produce a degree of obstruction, at least in the involved tubules.

CASE REPORTS

Case 1.-An infantryman suffered a perforating woundof 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 moreelapsed before his admission to a field hospital. At this time, the bloodpressure was unmeasurable, He was given 500 cc. of plasma and 2,500 cc. of lowtiter group O blood prior to operation. A catheterized specimen of urineappeared blood stained. A laparotomy was performed 7 hours after admission and24 hours after the wound had been incurred, and a laceration of the jejunum andearly severe peritonitis were observed. The laceration was sutured; theperitoneum was irrigated with isotonic solution of sodium chloride and 100,000units of penicillin; and 10 gm. of sulfanilamide were deposited in theperitoneal cavity. The wound at the left hip, which had produced a compoundfracture of the greater trochanter, was debrided. He was then given 5 gm. ofsodium sulfadiazine intravenously. Treatment with penicillin, 25,000 units every3 hours, was started on admission. The blood pressure at the endof operation was unmeasurable, but within 2 hours it rose to 100 systolic and 80diastolic. His postoperative course was characterized by progressive oliguria,edema, uremia, disorientation, and respiratory distress. Death occurred on theeighth postoperative day. On the first postoperative day, he received 500 cc. ofblood, 500 cc. of plasma, 1,000 cc. of dextrose in isotonic solution of sodiumchloride, and 5 gm. of sulfadiazine. On the second postoperative day, he wasgiven 500 cc. of blood, 2 units of plasma, 2,000 cc. of dextrose in isotonicsolution of sodium chloride, and 5 gm. of sulfadiazine. No more sulfadiazine wasgiven and no more blood except 1 pint (about 473 cc.) the day before death. Twodays before death, the nonprotein nitrogen in the blood was 91 mg., chlorides605 mg., and sulfadiazine 13.23 mg. per hundred cubic centimeters. His urinaryoutput on the day of operation was 150 cc., and on successive days it was 200cc., 350 cc., 300 cc., 600 cc., 400 cc., undetermined, and 75 cc.

At autopsy, the peritoneal cavity contained a small amount ofthick grayish yellow foul-smelling pus, and the viscera were plastered to oneanother 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 wastense beneath the sheet of exudate on its surface. On sectioning, the cutsurface was nutmeg brown, with well-defined architectural units. The spleen wasdoubled in size, and the capsule beneath the exudate was grayish red. Thekidneys were moderately enlarged; the capsules stripped readily, revealingsurfaces which were darker brown than normal, with fine dark red points andlines scattered throughout.

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The cortices were slightly widened; the pyramids were swollenand discolored by brown and red lines paralleling the tubules. The apexes of thepyramids were dark brownish yellow. The lungs did not collapse normally, andtheir weight was decidedly increased, particularly on the right side. Cutsurfaces were moist and released blood-stained mucoid fluid on pressure. Therewere slightly firm purplish red areas scattered throughout all the lobes, butthese were confluent only in the lower parts of the right upper and right lowerlobes. Examination of the renal sections showed that the glomeruli weremoderately congested; the tubules were slightly dilated. The distal convolutedand collecting tubules contained numerous brown granular and hyaline casts. Manytubules contained desquamated epithelial cells and polymorphonuclear cells. Onetubule showed a decided proliferative reaction interspersed withpolymorphonuclear cells. Here the inflammatory process extended into theinterstitium. There were scattered crystals of a sulfonamide drug within thelumens of the distal tubules. The interstitial tissues contained engorged bloodvessels, and there was extravasation of small red cells. Microscopic pathologicdiagnoses included pigment nephrosis, hemorrhagic bronchopneumonia, acutepurulent perihepatitis, and perisplenitis.

Case 2.-A 21-year-old soldier was injured during abombing raid when a stone building collapsed on him. He was extricated frombeneath a pile of stone after 3²/3hours and reached an evacuation hospital 15 minutes thereafter. There was novisible evidence of traumatism, and skeletal roentgenograms revealed nothing ofsignificance. His blood pressure was 104 systolic and 74 diastolic, and thepulse rate was 120. The urine was wine colored, with no red cells. Approximately7 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. Atransfusion was started, but when the hematocrit was observed to be 70 percentit was discontinued, after 300 cc. were given, and dextrose with isotonicsolution of sodium chloride substituted. The blood pressure rose to 100 systolicand 80 diastolic. A specimen of urine was chocolate colored. He complained ofmany points of muscular soreness and tenderness, and the areas were tense andbrawny on palpation.

During the succeeding 9 days, he remained oliguric, the dailyoutput of urine ranging from 50 to 100 cc., with an intake of about 3,000 cc. offluid. Sodium bicarbonate was given daily in 2.5 percent of solution. The patchymuscular induration increased. The urine became normal in color on the third daybut still had a positive benzidine reaction. On the sixth day, the face waspuffy, and there was pitting edema over the sacrum. The blood pressure was 150systolic and 110 diastolic. Magnesium sulfate was given intramuscularly. Duringthe next 3 days, the edema increased and the hypertension persisted; epistaxisbecame frequent; and death occurred with relative suddenness a little less than10 days after the injury. The level of nonprotein nitrogen in the blood reacheda total of 291 mg. and creatinine 12.2 mg. per hundred cubic centimeters the daybefore death occurred. A check for myoglobin on one specimen of urine earlyshowed a concentration of 588 mg. per hundred cubic centimeters. At autopsy, allmuscles appeared paler than normal and scattered throughout the skeletalmusculature were many focal areas of traumatic damage. In most instances, thesewere segments of muscles closely proximate to bone. Larger foci noted were inthe flexor group of the left forearm, the left vastus medialis, the lowerquarter of the right sartorius, and all of the right soleus. The general patternwas a pigmented grayish white area in the muscles surrounded by a hemorrhagicborder. Some of these areas appeared translucent and like fish flesh; otherswere frankly necrotic, with an opaque slighty grayish infiltration. Some fociappeared almost chalky, and the muscle fibers in the involved areas were friableand easily torn. The kidneys weighed 550 gm. They were symmetrically enlarged,and the vessels of the perirenal fat were engorged. One focus of hemorrhage inthis fat was noted at the lower pole of the right kidney. It was entirelyextracapsular. The capsules stripped readily and left pale smooth surfaces. Thearteries and veins were patent. On sectioning, the cortex was pale and swollen.The surfaces appeared moist;

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the pyramids were dark, with a hint of brown in predominantredness. The vessels were not engorged, and no gray zone was present at thecorticomedullary junction.¹⁷

Case 3.-A soldier was wounded in action near Cassino,Italy, by artillery shell burst. He was admitted to an evacuation hospitalapproximately 4? hours later, in good condition and showing no signs ofsignificant 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 operatingtent, the wound of entrance overlying the head of the left femur posteriorly wasdebrided, 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 theleft forearm was then debrided and the foreign body removed. Both wounds weretreated with sulfanilamide powder and petrolatum-impregnated gauze. During theoperation with the patient under gas, oxygen, and ether anesthesia, a bloodtransfusion was started. Later, while the patient was still on the operatingtable and still under anesthesia, generalized shaking chill, or rigor, began.The transfusion was discontinued and 500 cc. of plasma given. The same blood wasmatched again and observed to be compatible, and the rest of it was administeredwithout untoward reaction. Following the operative procedure, a catheter wasinserted, and 120 cc. of dark blood-stained urine was obtained. From this timeon, a catheter was employed every 12 hours. The bladder was still empty after 24hours. His general condition remained essentially unchanged until approximately8 hours before death, when he became irrational, breathing became irregular, andincreasing pulmonary edema developed. He died approximately 72 hours followingoperation.

He had received no blood other than that previously noted. Inaddition to the aforementioned amount of sulfadiazine, he was given 8 gm. bymouth the first 24 hours but none thereafter. Post mortem, the gross examinationof the kidneys, ureters, and the bladder failed to reveal any abnormality;however, microscopic examination of the kidneys revealed nephrosis of the lowernephron.

Case 4.-A crush syndrome developed in a soldier,similar to the one presented in Case 3, except that there was no history of lowblood pressure at any time during the 4? days that he lived after injury.

Case 5.-A soldier suffered a perforating wound of thebrain, a penetrating wound of the left jaw, and a perforating wound of the rightshoulder. He was admitted to an evacuation hospital over 10 hours after thewound had been incurred. On admission, his blood pressure was 130 systolic and74 diastolic; the pulse rate, 78; and respiration, 20. A roentgenogram of theskull showed that a foreign body 1.6 cm. in size had perforated the skull in theleft parietal region, had passed through the parietal lobes, and had perforatedthe right frontal aspect of the skull, and had come to rest with the bonefragment before it under the scalp. A linear fracture, 12 cm. long, extendedbackward in the frontal bone on the left, from the depressed fracture entrance.The patient was comatose on admission. He exhibited palsy of the right seventhnerve and spasticity in all extremities. Debridement of the wound of the skulland the brain was performed about 6 hours after the patient's admission to thehospital. In addition, the wounds of the jaw and the shoulder were debrided. Hewas given 1,500 cc. of blood and 1,000 cc. of plasma during the operation. Heremained comatose until his death. He had a relatively high temperature, withincreased pulse rate and respiration. He received sodium sulfadiazineintravenously 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. Numeroussulfadiazine crystals were observed, particularly in the left renal pelvis. Hedied 7 days after he was wounded. Microscopic observations at

¹⁷The report of the microscopic study was not available in this case, but it may be said that essentially the same picture was seen in patients with crush injury as in those with pigment nephropathy resulting from transfusion, poisoning due to sulfonamide drugs, and wounds attended with severe shock.

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autopsy included indications of encephalomalacia,bronchopneumonia, and pigment nephrosis.

Case 6.-A soldier was wounded inaction by a high explosive shell fragment 1 or 2 days before admission to anevacuation hospital. The exact date and the time of his wounding on MountPorchia, Italy, were unknown. On admission, he was semistuporous and showedchanges in his reflexes, and the roentgenogram showed depressed fracture of theright parietal bone, with a large bone defect and fragments of bone and metallicforeign bodies driven into the right cerebral hemisphere. The operative risk wasconsidered 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 hydrochlorideapproximately 8 hours after his admission to the hospital. Partial craniectomy,with thorough debridement of the wound of the brain and dural repair, wasaccomplished. At termination of the operation, the patient was sent to the wardin satisfactory condition, with a blood pressure of 120 systolic and 70diastolic, 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 thesecond 24 hours. Subsequently, he received sulfadiazine, 6 gm. daily by mouth,through the eighth postoperative day. He also received one unit of concentratedplasma twice daily for 8 days and four blood transfusions postoperatively. Hewas never entirely rational or lucid, but at times he responded moderately wellto questions and talked coherently. Four days postoperatively, the patient had acrisis, characterized by clonic contractions of the right side of the body andface for a few seconds, followed by twitching for several minutes and a suddenrise of temperature to 107? F; the pulse rate was 160 and respirations, 52. Allsubsided quickly. His daily temperature, aside from this one episode, was from102? to 103? F. On the ninth postoperative day, the patient was much weakerand drowsier and responded poorly to questions. He showed hemiplegia and facialparalysis on the left side, which had been present all along, plus weakness ofseveral cranial nerves. Treatment with sulfadiazine was discontinued on thisdate, 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 causeof the jaundice was not clear. At post mortem examination, it was noted that thecommon duct and larger branches were not obstructed and that the gallbladder wasnot enlarged. On sectioning, the hepatic tissue appeared to be deeply jaundiced,and the appearance was somewhat suggestive of a diffuse necrotic process. Theparenchyma of both kidneys appeared to be within normal limits; the kidneys wereabout normal size, and the capsules stripped normally. The pelves of the kidneyswere stained with bile, and the mucosa contained numerous pinpoint hemorrhages.No crystals were evident. There were no signs of infection in the wound of thebrain. The diagnoses, based on gross pathologic studies, were nonobstructivejaundice, the cause of which was undetermined; bronchopneumonia; and hepatitis.The report of microscopic examination of the section of the liver was notavailable, 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 wascarefully studied, and his daily urinary output was over 1,000 cc., except onthe day of his death. It is perhaps incorrect to assume that hemoglobinuricnephropathy contributed to death in this case.

Case 7.-A soldier was admitted to afield hospital approximately 1 day after being wounded by enemy shellfire nearMontecatini, Italy. He suffered compound fractures of the left tibia and fibulain the middle third, a compound fracture of the left clavicle, a compoundfracture of the left scapula, and multiple penetrating wounds of the leftbuttock. All of his wounds were debrided under open drop ether anesthesia in thefield hospital. Six days later, he was evacuated to an evacuation hospital,where he died 1 hour and 20 minutes after admission. There was nothing furtherin his record concerning his clinical course. Post mortem examination was done,and it was observed that both kidneys were enlarged, that

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the cortex was pale and swollen and irregularin both kidneys, and that the capsule stripped easily. A diagnosis, based ongross pathologic studies, of nephrosis was made, the cause of which was unknown.There were no microscopic observations in this case. Also presented werebilateral pleural effusion, a hematoma in the upper lobe of the left lung, andpulmonary congestion and edema, as well as the wounds previously noted. Whilethere was no evidence of shock recorded, it probably should be stated that therecord was too inadequate to permit the conclusion that shock did not exist atone time or another.

The condition described as pigment nephropathy, or lowernephron nephrosis, occurs with a variety of conditions. In battle casualties,the renal damage is probably dependent on renal ischemia plus the excretion ofpigment. The renal ischemia is vasoconstrictive in origin and occurs in patientsin a state of shock and with related conditions. Whether or not thevasoconstriction is induced by a toxin elaborated from damaged tissues or byreflex vasomotor stimulation has not been definitely established. The pigmentexcreted may be myoglobin or hemoglobin. The source of the hemoglobin may befrom transfused blood, intravascular hemolysis, and probably from other sources.The role of infection has not been clearly defined and should be made thesubject of investigation. The influence of the various anesthetic agents shouldbe studied.

Treatment should be prophylactic. Shock should be combatedvigorously, with prompt restoration of the volume of blood to normal. Thisshould be accomplished with the proper medium, which for most battle casualtiesis whole blood. Treatment with oxygen is of value in combating anoxia, whichmust result from vasoconstriction in the renal circulation. Injudicious use ofsulfonamide drugs should be avoided, and discontinuance of their use inconditions predisposing to nephropathy should be considered. Dehydration shouldbe avoided when possible and otherwise corrected as promptly as possible.Thorough surgical removal of all devitalized tissue and foreign bodies andprovision of adequate drainage to infected areas is important.

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