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Chapter IV

Battle Casualties in Korea, Studies of the Surgical Research Team, Volume I

Studies of Adrenal Function in Combat and Wounded Soldiers*

Captain John M. Howard, MC, USAR
First Lieutenant John M. Olney, MC, USAR
First Lieutenant John P. Frawley, MSC, USAR
Captain Ralph E. Peterson, MC, USAR
Serfin Guerra
and
Corporal William H. Dibrell
with the Technical Assistance of
Corporal Joel R. Wolfe
Corporal Charles Adams
Corporal William Bohley

Introduction

The purpose of this study has been to survey the combat soldier for evidence of a metabolic disorder of adrenal origin. It has had as its primary purpose to survey the possibility that adrenal insufficiency might result from the chronic stress of combat.

The study was carried out on the Eastern Front of Korea during the months of January 1952 to April 1953. This was a period of stable tactical conditions; a time when our lines, strung out along a chain of mountain tops, were under enemy observation and daily artillery fire. Patrols and probing activities were fairly active but no major change in the main line of resistance occurred. Troop morale was fair and combat fatigue was infrequent. Obviously, nervous tension was not maximal; yet all the factors which might seem an essential background for a syndrome of chronic stress were present.

The study has been divided into four phases: first, study of the unwounded soldier in the rear area; second, the study of the unwounded combat soldier; third, the study of the soldier immediately after wounding; and fourth, the study of the severely injured soldier over a period of 7 to 14 days following injury. This study has been designed primarily to delineate the problems peculiar to the combat soldier. 


*Previously published in abbreviated form in Annals of Surgery 141: 314, 1955.


27

Studies of the Noncombat Soldier

Partially to obtain control values, a limited number of studies were made of soldiers in noncombat areas. The methods of analyzing the urine for corticosteroids,3, 6 and 17-ketosteroids,1, 8, 9 and the method of counting the circulating eosinophiles7 have been previously published.

1. Eosinophile counts were performed daily for 2 or 3 successive days on 11 soldiers in a noncombat area.

The results (Table 1) were distributed about a mean of 142 with a standard deviation of 67. The extremes were 42 and 315.

Table 1. Eosinophile Counts of Noncombat Troops

(cells per cubic centimeter) 

Subject

Day 1

Day 2

Day 3

No. 1

184

86

71

No. 2

264

251

---

No. 3

148

139

117

No. 4

243

314

315

No. 5

259

195

142

No. 6

75

42

97

No. 7

142

203

153

No. 8

178

234

---

No. 9

75

72

61

No. 10

97

120

---

No. 11

144

115

---

2. Twenty-four-hour urine collections were made daily for 3 days on four healthy soldiers in a noncombat area. The results of these studies (Table 2) demonstrate an average excretion of 17-ketosteroids of 13.6 mg. with a range of 9.9 to 21.9 mg. All were within the limits of normal previously described as 8.0 to 22.0 mg. The excretion of corticosteroids (formaldehydogenic compounds) averaged 2.0 mg. per day with one individual excreting as much as 4.4 mg. per day. The normal excretion as described for this method is 0.6 to 2.6 mg. per day. The soldier who demonstrated the increased excretion of corticosteroids was under a marked emotional stress throughout the period of study. He was not a suitable subject for a control study but demonstrated at reaction not infrequently observed among men in combat areas.


28

Table 2. Steroid Excretion in Urine of Noncombat Soldiers in Korea

Subject

Day

Urine Volume cc.

17-Ketosteroids mg. per 24 hrs.

Corticoids* mg. per 24 hrs.

No. 1

1
2
3

750
800
740

15.1
19.0
16.6

1.4
0.9
2.4

No. 2

1
2
3

700
600
600

10.9
11.1
10.5

1.6
1.7
1.5

No. 3

1
2
3

900
700
800

21.9
9.9
12.0

3.1
2.7
4.4

No. 4

1
2
3

600
1,000
800

11.1
13.7
11.3

1.6
3.3
2.2


Average of 12 days

 

749

13.6

2.0

*Formaldehydogenic.

Studies of the Combat Soldier

To confirm the fact that these studies were carried out under conditions of potential stress, it should be noted that one of the subjects was killed in action during the period of observation and several others had their bunker destroyed by artillery fire. Furthermore, the study was interrupted several times by the infiltration of the United Nations lines by enemy troops or by the concentration of small arms fire. Again, no major, sustained battle occurred during the period of this study.

A. Eosinophile Counts

As part of a study of the physiologic response to the chronic stress of combat duty, a limited series of eosinophile counts was performed on a group of men in the front lines. It is recognized that the behavior of the circulating eosinophile in a chronic status is not sufficiently well defined to allow definite conclusions to be drawn, but it was hoped that such a relatively simple examination might provide preliminary insight into the problem.

Results

1. The counts of 21 men were obtained by a cooperating battalion surgeon in a station a mile behind the lines as the men left the front


29

line for 24 hours of rest. Each man had one count. The results were distributed about a mean of 87 with a standard deviation of 40. The extremes were 22 and 194 with the exception of one man whose count was 1,666. No further studies were made on this man except that a smear showed 25 per cent eosinophiles.

2. The counts of 17 men were obtained by a member of the research team. His equipment was set up behind a tank a few yards behind the ridge that formed the main line of resistance and the men reported there and returned directly to the area. Each man was examined on three consecutive days, their final count being the average of the three. The results were distributed about a mean of 154 with a standard deviation of 59. The extremes were 71 and 475 with the exception of one man whose counts on 3 days were 1,035, 1,227 and 822. This man was brought to the rear area where no indication of allergy or parasitic infestation could be found. His 24-hour excretion of corticosteroids (2.2 mg.) and 17-ketosteroids (11.6 mg.) was normal. On administration of ACTH, 25 mg. I. M., his eosinophile count dropped from 1,278 to 662. Three men in this study went on an uneventful combat patrol before or during the period of study. No change in their counts was observed.

The difference between the means of these two groups is statistically significant. The technic used in the first group was not, however, checked against that of members of the research team, and in view of the difficulties encountered in establishing a consistent technic, no further significance can be attached to the observation.

B. Studies of Adrenal Steroid Excretion

Three groups of front line soldiers were included in this study. With the aid of the company medical corpsman, volunteers were selected for study. Twenty-four-hour urine collections were made without otherwise breaking the daily routine of the subjects under study. Urine was preserved with toluene and refrigeration. Aliquots were shipped via air courier to the Department of Biochemistry, Army Medical Service Graduate School, for analysis.

References to Tables 3, 4 and 5 reveal that the 17-ketosteroid excretion was essentially normal. The corticosteroid (formaldehydogenic compounds) excretion varied from day to day. On some days the excretion was normal, on some days it was definitely elevated (600 per cent). No subnormal levels of the latter fraction were encountered. The day-to-day changes in excretion could not always be correlated with the day's activities although one study suggested a rather definite correlation (Table 4).


30

Table 3. Adrenal Steroid Excretion in the Combat Soldier

32nd Regiment, 7th Division, January 1952

Soldier

Urine Volume cc.

17-Ketosteroids mg. per 24 hrs.

Corticoids mg. per 24 hrs.

No. 10

1,850

2.5

18.7

No. 10

850

22.6

3.2

No. 10

450

7.4

7.1

No. 1

750

15.6

2.2

No. 1

1,200

15.1

3.3

No. 1

1,100

16.8

6.0

No. 2

450

8.2

1.0

No. 3

1,150

21.7

1.3

No. 3

1,250

22.1

2.6

No. 3

1,500

28.0

2.0

No. 4

650

16.2

1.3

No. 5

1,150

5.1

5.9

No. 5

1,000

13.6

2.4

No. 5

1,250

14.4

3.2

No. 6

1,000

14.7

2.4

No. 6

850

14.0

3.7

No. 7

650

5.8

2.1

No. 7

1,200

26.6

8.3

No. 8

500

8.5

2.1

No. 8

850

13.0

12.5

No. 9

1,200

16.4

2.5

Table 4A. Adrenal Steroid Excretion in the Combat Soldier*

3rd Battalion, 27th Regiment, 25th Division, May 1952 

Soldier

Rank

Age

Urine Volume cc.

17 Ketosteroid mg. per 24 hrs.

Corticoids mg. per 24 hrs.

Activity**

No. 1

1st Lt.

29

1,075

17.0

3.9

Normal day.

No. 1

1st Lt.

29

1,275

15.2

6.3

Normal day.

No. 1

1st Lt.

29

900

17.1

2.0

Night patrol.

No. 2

Pvt.

18

910

11.0

6.2

Normal day.

No. 2

Pvt.

18

1,000

15.9

2.1

Normal day.

No. 2

Pvt.

18

950

14.1

2.1

Normal day.

No. 3

2nd Lt.

26

1,450

10.8

4.4

Normal day.

No. 3

2nd Lt.

26

800

15.2

1.0

Normal day.

No. 4

M/Sgt.

34

2,600

16.8

5.3

Heavy mortar fire.

See footnotes at end of table.


31

Table 4A. Adrenal Steroid Excretion in the Combat Soldier*-Con.
 

Soldier

Rank

Age

Urine Volume cc.

17 Ketosteroid mg. per 24 hrs.

Corticoids mg. per 24 hrs.

Activity**

No. 4

M/Sgt.

34

2,050

11.0

6.2

Normal day.

No. 4

M/Sgt.

34

1,200

12.2

1.5

Normal day.

No. 5

Pfc.

21

1,250

8.2

5.9

Heavy mortar fire.

No. 6

Cpl.

28

1,100

12.4

6.0

Heavy mortar fire.

No. 7

Pvt.

21

1,000

14.8

5.5

Heavy mortar fire

No. 7

Pvt.

21

800

9.7

3.1

Heavy mortar fire.

No. 7

Pvt.

21

1,100

14.5

2.0

Heavy mortar fire.

No. 8

Pvt.

21

775

7.5

4.5

---

No. 8

Pvt.

21

900

13.9

2.1

Night patrol.

No. 9

Cpl.

21

2,500

12.8

9.4

Normal day.

No. 9

Cpl.

21

1,350

9.5

4.3

Normal day.

No. 9

Cpl.

21

600

7.8

1.1

Normal day.

No. 10

Pvt.

23

1,400

19.6

4.9

Normal day.

No. 10

Pvt.

23

1,100

13.1

1.2

Normal day.

No. 11

Pvt.

18

1,200

14.3

8.6

Normal day.

No. 12

Pvt.

22

1,100

10.7

8.6

Normal day.

No. 12

Pvt.

22

850

14.8

1.0

Normal day.

No. 13

Pvt.

22

800

13.7

2.6

Heavy mortar fire.

No. 13

Pvt.

22

800

15.4

1.0

Normal day.

No. 13

Pvt.

22

700

14.0

1.0

Normal day.

No. 14

Cpl.

22

700

11.4

1.6

Normal day.

No. 14

Cpl. 

22

425

9.4

1.1

Night patrol.

No. 15

Pvt.

21

1,300

10.8

9.2

Heavy mortar fire.

*All men on front line 40 days previously.
**As described by the individual soldier. Actually each was under the same general conditions as the other members of the group except for patrol activity (Table 4B).


32
 
Table 4B. Combat Stress*

Corticosteroid Excretion** by Combat Soldiers (Milligrams per 24 hours)

Date

Activity

1

2

3

4

5

6

7

8

9

10

11

12

13

14

15

11 May 1952

Heavy artillery fire

3.9

6.2

---

5.3

5.9

5.0

5.5

---

9.4

4.9

8.6

8.6

2.6

---

9.2

12 May 1952

Fewer incoming shells

6.3

2.1

4.4

6.2

---

---

3.1

4.5

4.3

---

---

---

1.0

1.6

---

13 May 1952

Rain-quiet

---

---

---

---

---

---

---

---

---

---

---

---

---

---

---

14 May 1952

Quiet day

2.0

2.1

1.0

1.5

---

---

2.0

2.1

1.1

1.2

---

1.0

1.0

1.1

---

*All men on front line for previous 40 days.
**Normal 0.6 to 2.6 mg. per day.


33

Table 4C. Combat Stress-All Men on Front Line

40 Days. A Study of 15 Soldiers

Date

Activity

Average Corticosteroid Excretion* mg. per 24 hrs.

11 May 1952

Heavy artillery fire

6.3 mg.

12 May 1952

Fewer incoming shells

3.7 mg.

13 May 1952

Rain-quiet

---

14 May 1952

Quiet day

1.5 mg.

*Normal range 0.6 to 2.6 mg.
 

Table 5. Adrenal Steroid Excretion in the Combat Soldier

1st Battalion, 27th Regiment, 25th Division, June 1952

Soldier

Rank

Age

Days on Line

Urine Volume cc.

17-Ketosteroids mg./25 hrs.

Corticoids mg./25 hrs.

Activity

No. 1

Pvt.

21

43

1,200

16.5

1.4

Normal activity.

No. 1

Pvt.

21

43

750

7.2

---

Heavy mortar fire.

No. 1

Pvt.

21

43

900

12.4

1.9

Nearby ambush. Two killed.

No. 2

Pfc.

23

2

1,400

18.0

1.6

Normal activity.

No. 2

Pfc. 

23

2

1,150

19.8

2.8

Heavy mortar fire.

No. 2

Pfc.

23

2

1,100

20.1

2.1

Nearby ambush. Two killed.

No. 3

Pvt.

18

40

3,200

30.2

2.1

Normal activity.

No. 3

Pvt.

18

40

800

12.3

2.9

Heavy mortar fire.

No. 3

Pvt.

18

40

900

20.4

2.1

Nearby ambush. Two killed.

No. 4

Pvt.

23

15

525

6.2

1.1

Normal activity.

No. 4

Pvt.

23

15

1,200

15.1

3.4

Heavy mortar fire.

No. 4

Pvt.

23

15

900

14.1

2.9

Nearby ambush. Two killed.

No. 5

Pfc.

20

79

600

11.9

0.9

Normal activity.

No. 6

Cpl.

24

81

2,000

15.9

2.0

Normal activity.

No. 7

Pfc.

23

81

900

12.4

0.7

Normal activity.


34

Studies Immediately After Injury

This phase of the study consisted of performing eosinophile counts on 63 wounded soldiers. It was designed to study the men immediately after injury so as to answer the question as to whether, under these circumstances, the normal adrenal response to injury was elicited. Does combat stress produce an adrenal cortical insufficiency to such an extent that the adrenal cannot respond following trauma?

Sixty-four casualties, wounded in action, were examined immediately on admission to the MASH. The eosinophile count was followed until it dropped or until it was felt that the count was no longer valid. Because of the possibility that the transfusion of banked blood (10 to 18 days old) might reduce the count, those observations made after transfusion of 4 pints of blood are indicated by an asterisk and those after 8 pints omitted. For presentation the patients are divided into three groups. Group 1 represents those with minimal wounds including one or more superficial perforating wounds (Table 6). These men could be ambulatory and were usually débrided under local anesthesia. Group 2 represents those with moderate to severe wounds (Table 7), and Group 3 represents those with near fatal or fatal wounds (Table 8). Of the six in the latter group, two died in surgery and two postoperatively.

As Table 6 indicates, the casualties of Group 1 usually had a significant drop in their eosinophile count. Occasionally, however, this was not true. It would appear that their trauma was not sufficient to reach the threshold for stimulating adrenal activity. On the other hand, the patients of Groups 2 and 3 uniformly responded with a significant drop within 4 hours after wounding. One patient of Group 2 is separately identified in the table. Casualty No. 10 had a single penetrating wound of the chest. Although there was never roentgenologic evidence of intrathoracic injury, the fragment apparently entered the pleural cavity and the patient was accordingly classed in Group 2 rather than Group 1.

Studies of sodium and potassium concentrations in the urine were performed on 31 seriously injured casualties on admission to the hospital. Hourly collections of urine were taken serially and the concentration of sodium and potassium was determined. The patients received only blood or 5 per cent glucose in water during the period of observation.

Figure 1 demonstrates the timing in the changes which were noted in three such patients as the adrenal cortical response occurred. Sodium conservation and potassium diuresis were demonstrated by the development of a sodium-potassium ratio of less than 1 in 27 of the


35

31 patients during the first few hours after injury. The exceptions were two with terminal injuries of the brain and spinal cord, one with a traumatic amputation who demonstrated the electrolytic reversal to a lesser extent and one casualty with a traumatic amputation of a leg who demonstrated no evidence of sodium conservation during a period of 10 hours after
injury. This study therefore offers further evidence of an adrenal response immediately after injury and manifesting itself at the time of admission to the hospital, 3 to 5 hours after wounding.

FIGURE 1.
Note the early conservation of sodium and excretion of potassium by the kidneys as demonstrated by
the development of a ratio of concentration of sodium: potassium of less than one.


36

Table 6. Eosinophile Counts in the Wounded Soldier
(cells per cubic centimeter)
Group 1. Minimally Injured

Casualty

Wound

Time Lag (hours)

Count

Time Lag (hours)

Count

Time Lag (hours)

Count

No. 1

Shell fragment, back

2.8

222

3.3

145

7.0

159

No. 2

Shell fragment wounds of extremities

2.8

56

3.8

95

7.3

62

No. 3

Superficial wounds of face and chest

6.8

97

8.5

131

12.3

37

No. 4

Shell fragment wounds of forearms and back

1.5

42

 

 

 

 

No. 5

Shell fragment wounds of back and buttock

3.3

9

 

 

 

 

No. 6

Shell fragment, back

3.8

11

 

 

 

 

No. 7

Minimal shell fragment wound of forearms

3.8

61

 

 

 

 

No. 8

Minimal shell fragment wound of back

3.5

17

 

 

 

 

No. 9

Minimal shell fragment wound of calf

 4.5

 25

 5.5

72

 

 

No. 10

Superficial shell fragment wounds of chest and extremities

3.3

72

4.8

55

17.5

57

No. 11

Shell fragment, back and thigh

2.3

56

4.0

22

 

 

No. 12

Superficial shell fragment wounds of chest and extremities

4.8

50

 

 

 

 

No. 13

Superficial shell fragment wounds of extremities

11.8

37

 

 

 

 

No. 14

Shell fragment wounds of extremities

3.8

26

 

 

 

 

No. 15

Shell fragment wounds of thigh

1.5

177

4.0

47

 

 

No. 16

Shell fragment wounds of extremities

4.3

2

 

 

 

 

No. 17

Superficial shell fragment wounds of chest and extremities

5.5

2

 

 

 

 

No. 18

Shell fragment, neck

4.8

30

 

 

 

 


37

Table 7. Eosinophile Counts in the Wounded Soldier

Group 2. Seriously Injured 

Casualty

Wound

Time Lag (hours)

Count

Time Lag (hours)

Count

Time Lag (hours)

Count

No. 1

Perforation of chest

2.0

44

4.5

11

 

 

No. 2

Traumatic amputation of foot

4.5

14

4.8

8

 

 

No. 3

Multiple shell fragment wounds

1.8

14

 

 

 

 

No. 4

Traumatic amputation of fingers

2.0

48

3.5

44

5.3

2

No. 5

Perforating shell fragment wounds of extremities

2.0

36

 

 

 

 

No. 6

Bullet wound of maxilla, fracture of humerus

4.3

0

 

 

 

 

No. 7

Large perforating wound of thigh

1.5

3

 

 

 

 

No. 8

Perforating wound of thighs and legs

3.3

6

 

 

 

 

No. 9

Shell fragment wounds of feet, thigh, chest

4.8

156

5.8

92

11.5

33

No. 10

Perforating wound of chest

4.3

164

 

 

 

 

No. 11

Perforating wound of neck, chest

4.0

0

 

 

 

 

No. 12

Perforating wound of kidney, chest

1.5

60

4.0

0*

 

 

No. 13

Perforating wound of lung and arm

2.8

11

 

 

 

 

No. 14

Traumatic amputation of foot, multiple soft tissue wounds

1.5

69

2.5

9*

 

 

No. 15

Perforation of back, stomach, liver

3.0

23

 

 

 

 

No. 16

Perforation of liver

1.8

76

6.0

25*

 

 

No. 17

Severe shell fragment wounds of leg

1.5

61

 

 

 

 

No. 18

Penetrating shell fragment wound of abdomen

8.0

2

 

 

 

 

No. 19

Penetrating shell fragment wound of chest

5.5

0

 

 

 

 

No. 20

Penetrating shell fragment wounds of face, thigh, knees

4.3

12

 

 

 

 

*After receiving blood.


38

Table 7. Eosinophile Counts in the Wounded Soldier-Continued

Group 2. Seriously Injured-Continued 

Casualty

Wound

Time Lag (hours)

Count

Time Lag (hours)

Count

Time Lag (hours)

Count

No. 21

Large shell fragment wound of thigh

5.8

2

 

 

 

 

No. 22

Traumatic amputation of leg

5.0

3

 

 

 

 

No. 23

Traumatic amputation of both legs

5.0

0

 

 

 

 

No. 24

Traumatic amputation of leg

2.0

183

4.0

22

 

 

No. 25

Traumatic amputation of foot

9.0

0

 

 

 

 

No. 26

Traumatic amputation of foot

3.0

17

 

 

 

 

No. 27

Shell fragment wound of chest, legs

8.3

0

 

 

 

 

No. 28

Traumatic amputation of foot

7.5

0

 

 

 

 

No. 29

Penetrating wounds of extremities

6.3

0

 

 

 

 

No. 30

Penetrating wound of abdomen

6.0

0

 

 

 

 

No. 31

Multiple shell fragment wounds of extremities

5.5

0

 

 

 

 

No. 32

Multiple shell fragment wounds of scalp, knee and back

6.5

0

 

 

 

 

No. 33

Perforating wounds of arm, face, orbit

2.5

6

 

 

 

 

No. 34

Wounds of arm, face and thigh

3.0

0

 

 

 

 

No. 35

Multiple shell fragment wounds of orbit, face, extremities

3.5

0

 

 

 

 

No. 36

Perforating wound of chest

3.3

0

 

 

 

 

No. 37

Large wound of back

6.0

0

 

 

 

 

No. 38

Penetrating wound of ankle

6.8

10

 

 

 

 

No. 39

Multiple wounds of extremities

3.8

10

 

 

 

 

No. 40

Multiple shell fragment wounds of face and extremities

8.3

0

 

 

 

 


39

    Table 8. Eosinophile Counts in the Wounded Soldier
    (cells per cubic centimeter)
    Group 3. Critically Injured

Casualty

Wound

Time Lag (hours)

Count

Time Lag (hours)

Count

Time Lag (hours)

Count

No. 1

Perforation of small bowel, colon, iliac vessels; died during operation.

1.8

73

 

 

 

 

No. 2

Perforations of abdomen, heart, extremities; died during operation.

1.8

34

 

 

 

 

No. 3

Compound fractures of tibia and femur, bilateral, perforation of abdominal viscera; died postoperatively.

2.3

173

3.3

69*

7.0*

0

No. 4

Perforation of spleen, stomach, diaphragm, chest, severe shock.

2.0

126

3.0

19*

 

 

No. 5

Perforations of small bowel, massive soft tissue wounds, multiple fractures.

9.0

6

 

 

 

 

No. 6

Multiple perforations of bowel, perforation of vena cava, massive fractures.

1

66

6

1*

 

 

*After receiving blood.

Studies During Early Convalescence

Twenty battle casualties were chosen for study during a period of 7 to 14 days immediately after injury. This study was designed to analyze adrenal function during this period of early convalescence. This was a period of repeated traumas-initial injury, evacuation, anesthesia, operation, secondary dressings and secondary débridement. All of the patients studied were critically injured. Several died of their injuries or were evacuated because of post-traumatic renal insufficiency.

The study consisted of daily eosinophile counts at approximately 0800 hours, determination of daily urinary excretion of
17-ketosteroids


40

and corticosteroids, and balance studies of sodium and potassium. During the first week of convalescence, most of the patients were on intravenous fluids or on standard canned liquids. Intakes could be rather accurately determined during this period by measurement of intake and analysis of representative samples. During the latter part of a patient's study, representative servings of food were weighed and electrolyte content calculated from standard charts (Hospital Diets-Department of the Army Technical Manual 8-500). Thus intake measurements during the latter phase were, of necessity, less accurate than those of the earlier days. Urine, gastric drainage and other fluids excreted in significant quantities were measured and analyzed. In charting the balance studies, the day of injury and operation, although studied, was usually not graphed because the blood loss measurements were inaccurate. On the day of admission, whole blood and glucose were used almost exclusively. The 16 patients studied most intensively are presented as case reports.

Results

Analysis of the studies indicates again the response to repeated traumas. In response to the original trauma, or more correctly, in response to the continuous trauma of the day of injury, the corticosteroid (formaldehydogenic compounds) excretion rose. This increased excretion continued for 1 to 3 days and then subsided. The low rate of excretion was maintained for 1 to 2 days and was then sometimes followed by a secondary rise of lesser magnitude. Secondary trauma after the first 3 days was usually followed by an increased excretion of this fraction. Occasionally there was a late rise of considerable magnitude. The validity of this rise might be questioned, but in view of the repetition of the analysis and the constancy of the test in demonstrating an early rise, this occasional late "spontaneous" rise would appear valid. The only exception to the early increase in excretion was in a patient who was developing post-traumatic oliguria. Presumably, this failure in excretion of the steroids was renal in nature rather than adrenal. Dextran administration invalidates this determination.

The 17-ketosteroid excretion was seldom abnormal. It tended roughly to follow the corticosteroid fraction in a qualitative manner, but a rise above normal was infrequently observed.

Without exception, the eosinophile count fell with the original trauma. Thereafter the eosinophile count tended to be inversely proportional to the excretion of the corticosteroids. About the third to the fifth day, the concentration rose to a higher level, normal or above, and then fell again. Secondary trauma usually caused a secondary drop of short duration.


41

The balance studies demonstrate the selective conservation of sodium and the excretion of potassium. The point of interest in these studies is the magnitude and duration of these changes. The massive and repeated traumas sometimes maintained these phenomena throughout a period of 7 to 14 days.

Case Reports

Patient No. 1. This soldier, age 23 years, weight approximately 165 lbs., blood type A, had been in the front lines for 2 weeks prior to injury. While on patrol at 0230 hours, 18 February 1952, he was wounded by a land mine. The injuries included traumatic amputation of both legs at the level of the calf. Tourniquets were applied to the legs and the patient was given 1,000 cc. of blood, 200 cc. of albumin and 500 cc. of plasma at the battalion aid station.

He arrived via helicopter at the hospital 4 hours after injury. His blood pressure at this time was 120/80, pulse 96 and of good quality. He was pale, but his peripheral circulation seemed fairly good. After another 1,000 cc. of blood, his pressure rose to 140/80, pulse rate remaining 96 per minute. When his litter was moved to the operating room, 6 hours after injury, his pressure fell to 110/60. Re-amputation of the legs was performed under spinal anesthesia and required 1.5 hours. His course was smooth throughout the procedure except for a mild hypertension. Immediately after operation he was given his third liter of blood. Amputation was associated with a blood loss measured as 1,350 cc. There was no detectable blood loss thereafter.

On the ninth postoperative day, a secondary dressing was performed under pentothal, nitrous oxide anesthesia. The wounds appeared clean.

The blood given on the day of admission was type O, 21 to 22 days of age. During the subsequent course he was given a total of 2,500 cc. of fresh type-specific blood. By the fifth day post-injury, he was eating a liberal diet.

Discussion. This patient's course represents the response to uncomplicated trauma. The pattern of the corticosteroid excretion was one of an initial rise, with a secondary rise on the tenth day after secondary trauma (Fig. 2). The late rise, following a secondary insult, was of greater proportion than the original response. The height of the peak and its duration may be related not only to adrenal stimulation, but to the ability of the kidneys to excrete the steroids. This hypothesis is based on the studies which demonstrated a marked decrease in glomerular filtration after massive injuries.4

The 17-ketosteroid excretion remained normal throughout his course (Fig. 2). The eosinophile count fell to zero after trauma. As his corticosteroid excretion subsequently diminished, the eosinophile count rose to a peak of 540 per ml. on the fifth day post-wounding. This would appear to be a rather definite rebound phenomenon7 in which the count rose above normal. It rapidly fell thereafter and remained at a low normal level after the secondary operation. His oral temperature remained 98° to 100° throughout his course except for a spike to 103° on the seventh day.

He remained in positive sodium balance (Fig. 3) throughout the first 10 days of the study except for 1 day. On the fifth day he was in a slightly negative sodium balance. This was the day on which his eosinophile count reached its peak and was one of the days on which the corticosteroid excretion was very low. On the eighth day his balance was almost zero, but he swung back to sodium conservation for 2 days after the secondary anesthesia. During the


42

FIGURE 2.
Demonstrating the normal excretion of 17-ketosteroids, the increase in excretion of corticosteroids after the primary and secondary operative traumas, and the fall and rebound phenomena in circulating eosinophile concentration.

first 11 days after injury, therefore, his cumulative sodium retention was approximately 290 mEq. (Fig. 4).

He developed a negative potassium balance for 2 days which again became more pronounced after the secondary trauma. On the eleventh day, the day of the maximal corticosteroid excretion, his potassium loss was also maximal (Figs. 2, 3). Thus his cumulative potassium loss was approximately 355 mEq. during the first 11 days (Fig. 4). The plasma sodium concentration fell rapidly over a few hours from 141 to 122 mEq. per liter and during the course of the study never reached a normal concentration again in spite of the sodium conservation. In contradistinction, the potassium diuresis was associated with a slight rise in the plasma concentration of potassium after the secondary injury (Fig. 5).

Figure 6 demonstrates water conservation early followed by a diuresis which was only transiently checked by the secondary anesthetic trauma. Thereafter the diuresis continued in spite of the adrenal hyperactivity.

Patient No. 2. A 21-year-old American soldier, weight 135 lbs., blood type B, in combat 2 weeks, in Korea 31/4 months.


43

FIGURE 3.
Demonstrating the early conservation of sodium and excretion of potassium following trauma. This trend was spontaneously reversed but again appeared to be exaggerated by the secondary operative (anesthetic) trauma on the ninth day. These charts are constructed so that the height of the column above the zero line represents intake (indicated by the figure above the column). The figure in the column represents output and the shaded area and the figures below the column represent the positive or negative balance (after Moore).
 

This soldier was wounded by fragments from a land mine at 0230 hours, 18 July 1952, while on patrol duty. His injuries included a traumatic amputation of the lower left leg and extensive soft tissue injuries of the right calf.

He arrived via litter and litter jeep at the battalion aid station at 0455 hours and via helicopter at the hospital at 0630 hours. No resuscitative measures were recorded during this time beyond control of hemorrhage. On admission to the hospital his blood pressure was 150/80, pulse rate 100. His pulse was of good quality, and his color was normal. He was quiet and alert.

Re-amputation of the left leg and débridement of the right leg were completed under spinal anesthesia by 0835 hours. During this time he received 850 cc. of type O bank blood (22 days of age). Subsequent transfusions were of fresh, type-specific blood, locally obtained. During operation his blood pressure ranged about 100/50, pulse 100, respirations 20 per minute. His operative blood loss, as measured by the washed sponge technic, was 450 cc. His postoperative


44

FIGURE 4.
On the eleventh day after the original injury, the patient was still losing potassium
and had barely begun to excrete the retained sodium.

course was marked by the development of fever on the third day. Spinal anesthesia was repeated for secondary dressings on the second postoperative day, for redébridement on the sixth postoperative day and for re-amputation of the left leg on the tenth day. The re-amputation was necessary because of gangrenous muscle at the level of the previous amputation. Oral diet was repeatedly supplemented with intravenous fluids.

Discussion. This study is primarily a study of repeated traumas. Three secondary operations were performed on the second, sixth and tenth days post-injury. On the second day post-injury, the original adrenal response was still manifested and no further response was detectable. Following the latter two operations, a sharp response occurred in each instance.

This soldier is one of two studied who had residual necrotic tissue. The necrotic tissue in the wounds of this casualty was not extensive. Reference to Figure 7 indicates that his eosinophile count fell to zero and then rapidly rose, finally to reach the very high level of 840 on the eighth day. Following secondary débridement on the sixth day, and possibly unrelated, there was a late fall coincident with a secondary rise in corticosteroid excretion. The corticosteroid excretion remained elevated throughout 5 days of study prior to the secondary débridement of the wounds. It then fell to normal, but again became elevated after secondary operations on the sixth and tenth days. The 17-ketosteroid excretion was not elevated.

Daily balance studies (Figs. 8, 9) demonstrated a tendency to conserve sodium until the eighth day after injury. He then developed a negative sodium balance


45

FIGURE 5.
Demonstrating the marked fall in plasma concentration following
the original sequence of traumas.

FIGURE 6.
The early conservation of water was followed by a
diuresis on the tenth and eleventh days.

which was reversed by secondary trauma. This reversal, following secondary trauma on the tenth day, was coincident with a sharp reversal in the diuresis (Fig. 10) which had roughly paralleled his sodium balance. His cumulative sodium balance is indicated in Figure 11. Potassium loss followed the primary injury and the secondary injuries on the second and tenth days (Fig. 9). His cumulative potassium loss was therefore increasing at the time of his evacuation on the twelfth day (Fig. 12). Figure 13 demonstrates a very sharp decrease


46

FIGURE 7.
Demonstrating the effect of necrotic tissue in producing a continued stimulus to corticosteroid excretion.
Repeated traumas produced delayed but repeated responses in corticosteroid excretion.
Note the evaluation in the eosinophile concentration to 840 cells per ml. on the eighth day post-injury.
 

in the ratio of sodium-potassium excretion following each of the three secondary insults. Figure 14 demonstrates the trend to consistent, inverse changes in his plasma sodium and potassium concentration. Secondary trauma resulted in a sharp fall in plasma sodium and a slight rise in plasma potassium concentration.

Patient No. 3. A 21-year-old American soldier, weight 170 lbs., blood type O, in combat 2 months, in Korea 4 months.

This soldier stepped on a land mine near the battalion aid station at 1900 hours, 3 August 1952. His injuries included a perforation of the inferior vena cava, four perforations of the duodenum, eight perforations of jejunum and ileum, penetration of the chest, penetration of the left popliteal artery, shattering compound fractures of the left femur, left tibia, right tibia, and multiple soft tissue wounds of both lower extremities.

After 200 cc. of albumin at the aid station, he was evacuated by helicopter, arriving 1 hour after injury. He was cold, pale, restless, and the capillary refilling was slow. His blood pressure and pulse were unobtainable.

After 6 pints of blood his pressure was 100/60. After 9 pints of blood his pressure was 120/70, pulse 132.


47

FIGURE 8.
The prolonged period of positive sodium balance appears to be a response to repeated
traumas and perhaps to the continued injury resulting from necrotic tissue.

FIGURE 9.
Secondary traumas on the second day and on the tenth day
were reflected by a secondary potassium diuresis.


48

FIGURE 10.
Secondary operation on the tenth day reversed the diuresis.

Operation, lasting 4 hours, was begun 5 hours after injury. After a pentothal induction, ether and curare were utilized. The vena cava was ligated below the renal veins. The ileum was resected and multiple small bowel perforations were closed. Several soft tissue wounds were débrided. The popliteal artery was not bleeding externally, and because of the critical condition of the patient, the wound was not explored. For a short time during the operation, the blood pressure was unobtainable. For the last hour and a half the pressure ranged between 80/50 and 100/60. By the end of operation he had been given a total of 21 pints of type O bank blood, averaging 15 days of age. Operative blood loss was measured at approximately 4,000 cc. Postoperatively his pressure stabilized at 110/60 to 130/70 for 17 hours and then spontaneously rose to 160/90, pulse rate 130 per minute. Thereafter his pressure remained above 140/80 until his evacuation on his fourteenth postoperative day.

His postoperative course was febrile (101°-102°). Amputation below the left knee was necessary on the ninth day post-injury because of gangrene subsequent to the perforation of the popliteal artery.


49

FIGURE 11.
The cumulative retention of sodium reached 800 mEq.

FIGURE 12.
Potassium loss had not abated at the end of the eleventh day of study.


50

FIGURE 13.
Demonstrating the effect of repeated traumas on the urinary excretion of electrolytes.
The first two points represent preoperative and postoperative values.

FIGURE 14.
Three operations were each followed by a marked fall in plasma sodium
concentration and a slight rise in potassium concentration.


51

Discussion. This soldier had wounds which were almost fatal in extent. He developed gangrene of an extremity which was not amputated until the ninth day. Meanwhile, his corticosteroid excretion remained high and his eosinophile count was very slow to rise (Fig. 15). His eosinophile count fell transiently after the second operation. The 17-ketosteroid excretion was persistently low, among the lowest in the group studied. His potassium loss was the highest of any patient studied, reaching 480 mEq. (Figs. 16, 17). The loss was extremely high for the first 6 days after injury (Fig. 16), and then the balance became positive at the time his eosinophile count started to rise. His sodium retention (Fig. 18) was also the most marked, reaching 970 mEq. (cumulative) by the thirteenth day (Fig. 19). Sodium retention occurred throughout the 13-day period.

This patient, like the preceding one, demonstrates the changes associated with gangrenous tissue. This soldier had gangrene of an entire lower limb with an associated infection. The result was a continued stimulation of the adrenal cortex and a continued loss of potassium and retention of sodium. The potassium loss may have represented cell destruction in the gangrenous limb. This gangrenous limb, because of loss of cellular integrity, produced the equivalent of an increase in extracellular fluid space comparable to the volume of the gangrenous tissue. Thus in electrolytic equilibration, potassium would be lost and sodium retained in the nonviable tissue (Fig. 20).

With injury his plasma sodium concentration fell to 128 mEq. in spite of sodium retention. Thereafter it rose slowly only to fall again with the secondary operation. Coincident with the secondary operation, his plasma potassium rose as his sodium fell.

Patient No. 4. A 21-year-old American soldier, weight 155 lbs., blood type A, in Korea 2 months, and in the combat area the entire time.

This soldier was wounded at 0100 hours, 19 August 1952, by the explosion of an artillery shell. The injury consisted of shattering fractures of both femurs as well as fractures of the pelvis and extensive soft tissue injuries.

At the battalion aid station, 0315 hours, his blood pressure was 100/60. He was given albumin 100 cc., blood 1,000 cc., saline 1,000 cc., morphine 30 mg. followed 3 hours later by 8 mg.

On arrival at the hospital via helicopter at 0660 hours, his pressure was 82/40 and his condition appeared precarious. By 0920 hours, he had received 2,500 cc. of blood at the hospital. His pressure had risen to 165/96. With the onset of pentothal, nitrous oxide and ether anesthesia, his pressure fell to 105/60 with a pulse rate of 102 per minute.

Toward the end of operation the pressure fell to 82/42, pulse 124 per minute. Operation consisted of débridement and casting of the legs and required 11/4 hours. By the end of operation he had been given a total of 12 pints of blood. His pressure again fell to 80/50, pulse 160. He was then given an additional 6 pints of blood, 3 units of albumin, and 1,000 cc. of 5 per cent glucose in water. His pressure gradually rose to 112/55, pulse 148, respirations 20 per minute (1900 hours). Because the pressure again fell to 90/50 later during the night, another pint of blood and unit of albumin were given (total 19 pints of type O bank blood, 15 days of age, and 5 units of albumin).

His subsequent course was smooth. The blood pressure stabilized by the first postoperative day at 120/60, pulse 140. A secondary dressing was performed under spinal anesthesia on the fifth postoperative day. The wounds appeared clean.


52

FIGURE 15.
This casualty had a continuing injury in the form of a gangrenous leg. Note the persistent
absence of circulating eosinophiles and the persistent increase in the excretion of corticosteroids.
These changes were more marked than in any other patient. The excretion of 17-ketosteroids was not increased.

FIGURE 16.
Demonstrating the extremely rapid loss of potassium. Much of the potassium
may have come from the nonviable cells of the lower extremity.


53

FIGURE 17.
The potassium loss during the first 6 days was the
greatest encountered in any casualty.

FIGURE 18.
The sodium balance was positive throughout
the 2-week period of study.


54

FIGURE 19.
As with the potassium loss, the conservation of sodium
was the greatest of any casualty studied.

FIGURE 20.
The patient excreted more potassium than sodium for 7 days.


55

Discussion. This patient had at massive primary injury. His subsequent course was smooth. His corticosteroid excretion was elevated early and fell to normal limits on the third and fourth days post-injury (Fig. 21). This change was accompanied by the inverse changes in eosinophile concentration (Fig. 21) and sodium and potassium balances (Fig. 22). The secondary trauma on the fifth day post-injury was followed by only a slight response. The corticosteroid excretion was elevated again at the end of the 9-day study. This repeated adrenal response resulted in a continued conservation of sodium, reaching a level of 876 mEq. at the end of 7 days (Fig. 23).

In this casualty with a massive wound without necrosis the sodium retention approached that of the preceding casualty but the potassium loss did not. The difference is only partially explained on the basis of the loss of gastrointestinal fluids in the preceding patient. Tissue necrosis with superimposed infection appears to be a strong, continued stimulus of the adrenal cortex and of changes in electrolyte balance.

Patient No. 5. A 19-year-old American soldier, blood type O, in Korea 2 months, in combat 2 months.

This soldier was wounded at 1030 hours, 1 September 1952, by the explosion of a land mine. His injuries included traumatic amputation of both legs at the knee. He arrived at the battalion aid station 30 minutes later and was given 1,500 cc. of blood and 30 mg. of morphine.

On arrival at the hospital (via helicopter) at 1200 hours, his blood pressure was almost unobtainable. His radial pulse was faint. After 2,500 cc. of blood intravenously, his pressure was distinct at 60/50. Arterial transfusion was then begun and his pressure rose rapidly from 82/70 to 115/80 after the infusion of 3,500 cc. by this route. After 5s.

FIGURE 14.
Three operations were each followed by a marked fall in plasma sodium
concentration and a slight rise in potassium concentration.


51

Discussion. This soldier had wounds which were almost fatal in extent. He developed gangrene of an extremity which was not amputated until the ninth day. Meanwhile, his corticosteroid excretion remained high and his eosinophile count was very slow to rise (Fig. 15). His eosinophile count fell transiently after the second operation. The 17-ketosteroid excretion was persistently low, among the lowest in the group studied. His potassium loss was the highest of any patient studied, reaching 480 mEq. (Figs. 16, 17). The loss was extremely high for the first 6 days after injury (Fig. 16), and then the balance became positive at the time his eosinophile count started to rise. His sodium retention (Fig. 18) was also the most marked, reaching 970 mEq. (cumulative) by the thirteenth day (Fig. 19). Sodium retention occurred throughout the 13-day period.

This patient, like the preceding one, demonstrates the changes associated with gangrenous tissue. This soldier had gangrene of an entire lower limb with an associated infection. The result was a continued stimulation of the adrenal cortex and a continued loss of potassium and retention of sodium. The potassium loss may have represented cell destruction in the gangrenous limb. This gangrenous limb, because of loss of cellular integrity, produced the equivalent of an increase in extracellular fluid space comparable to the volume of the gangrenous tissue. Thus in electrolytic equilibration, potassium would be lost and sodium retained in the nonviable tissue (Fig. 20).

With injury his plasma sodium concentration fell to 128 mEq. in spite of sodium retention. Thereafter it rose slowly only to fall again with the secondary operation. Coincident with the secondary operation, his plasma potassium rose as his sodium fell.

Patient No. 4. A 21-year-old American soldier, weight 155 lbs., blood type A, in Korea 2 months, and in the combat area the entire time.

This soldier was wounded at 0100 hours, 19 August 1952, by the explosion of an artillery shell. The injury consisted of shattering fractures of both femurs as well as fractures of the pelvis and extensive soft tissue injuries.

At the battalion aid station, 0315 hours, his blood pressure was 100/60. He was given albumin 100 cc., blood 1,000 cc., saline 1,000 cc., morphine 30 mg. followed 3 hours later by 8 mg.

On arrival at the hospital via helicopter at 0660 hours, his pressure was 82/40 and his condition appeared precarious. By 0920 hours, he had received 2,500 cc. of blood at the hospital. His pressure had risen to 165/96. With the onset of pentothal, nitrous oxide and ether anesthesia, his pressure fell to 105/60 with a pulse rate of 102 per minute.

Toward the end of operation the pressure fell to 82/42, pulse 124 per minute. Operation consisted of débridement and casting of the legs and required 11/4 hours. By the end of operation he had been given a total of 12 pints of blood. His pressure again fell to 80/50, pulse 160. He was then given an additional 6 pints of blood, 3 units of albumin, and 1,000 cc. of 5 per cent glucose in water. His pressure gradually rose to 112/55, pulse 148, respirations 20 per minute (1900 hours). Because the pressure again fell to 90/50 later during the night, another pint of blood and unit of albumin were given (total 19 pints of type O bank blood, 15 days of age, and 5 units of albumin).

His subsequent course was smooth. The blood pressure stabilized by the first postoperative day at 120/60, pulse 140. A secondary dressing was performed under spinal anesthesia on the fifth postoperative day. The wounds appeared clean.


52

FIGURE 15.
This casualty had a continuing injury in the form of a gangrenous leg. Note the persistent
absence of circulating eosinophiles and the persistent increase in the excretion of corticosteroids.
These changes were more marked than in any other patient. The excretion of 17-ketosteroids was not increased.

FIGURE 16.
Demonstrating the extremely rapid loss of potassium. Much of the potassium
may have come from the nonviable cells of the lower extremity.


53

FIGURE 17.
The potassium loss during the first 6 days was the
greatest encountered in any casualty.

FIGURE 18.
The sodium balance was positive throughout
the 2-week period of study.


54

FIGURE 19.
As with the potassium loss, the conservation of sodium
was the greatest of any casualty studied.

FIGURE 20.
The patient excreted more potassium than sodium for 7 days.


55

Discussion. This patient had at massive primary injury. His subsequent course was smooth. His corticosteroid excretion was elevated early and fell to normal limits on the third and fourth days post-injury (Fig. 21). This change was accompanied by the inverse changes in eosinophile concentration (Fig. 21) and sodium and potassium balances (Fig. 22). The secondary trauma on the fifth day post-injury was followed by only a slight response. The corticosteroid excretion was elevated again at the end of the 9-day study. This repeated adrenal response resulted in a continued conservation of sodium, reaching a level of 876 mEq. at the end of 7 days (Fig. 23).

In this casualty with a massive wound without necrosis the sodium retention approached that of the preceding casualty but the potassium loss did not. The difference is only partially explained on the basis of the loss of gastrointestinal fluids in the preceding patient. Tissue necrosis with superimposed infection appears to be a strong, continued stimulus of the adrenal cortex and of changes in electrolyte balance.

Patient No. 5. A 19-year-old American soldier, blood type O, in Korea 2 months, in combat 2 months.

This soldier was wounded at 1030 hours, 1 September 1952, by the explosion of a land mine. His injuries included traumatic amputation of both legs at the knee. He arrived at the battalion aid station 30 minutes later and was given 1,500 cc. of blood and 30 mg. of morphine.

On arrival at the hospital (via helicopter) at 1200 hours, his blood pressure was almost unobtainable. His radial pulse was faint. After 2,500 cc. of blood intravenously, his pressure was distinct at 60/50. Arterial transfusion was then begun and his pressure rose rapidly from 82/70 to 115/80 after the infusion of 3,500 cc. by this route. After 5,000 cc. of blood at the hospital, his pressure was 142/100, pulse 136. Pentothal anesthesia was then begun (1440 hours) and the pressure fell to 98/50, pulse rate 140 per minute. With bilateral tourniquets in place, bilateral amputation was performed. The amputations were radical, high in the thigh, proximal to all visibly injured tissue. Of all patients studied, the débridement of this patient was perhaps the most radical and therefore the most complete. Nitrous oxide, oxygen and ether were used in addition to a total of 175 mg. pentothal.

Operation was completed at 1555 hours. His blood pressure never rose over 100 mm. systolic during the procedure and the pulse rate ranged about 130 to 140 per minute. By the end of the operation he had received 18 pints of blood (21 including that at the aid station). Three more pints immediately postoperatively raised the over-all total to 24 pints (type O, 12 days of age) on the day of injury. As he recovered consciousness, his pressure rose spontaneously to 160/100, pulse 90 to l00, respirations 20 per minute. Fifteen hours postoperatively his pressure had fallen to 110/75, pulse 94, respiratory rate 20 per minute.

With the tourniquets in place, external blood loss seemed hardly to have exceeded 3,000 cc. at the hospital. Postoperative bleeding was not noted.

Subsequently he was essentially afebrile and his course was exceedingly smooth. A total of 500 cc. of blood (fresh) was given on the second postoperative day and 1,000 cc. on the third day. A secondary dressing was performed on the third postoperative day under spinal anesthesia. His course for the next 2 months was reported as uneventful.

Discussion. This patient also represents a response to massive wounds of the extremities. The steroid collection on the first day after injury was lost so that the height reached during the first full 24-hour period is unknown.


56

FIGURE 21.
The corticosteroid excretion was quite high on the first day
and gradually fell to normal. Secondary anesthetic trauma was
associated with only a slight corticoid response.

FIGURE 22.
Sodium conservation was marked.


57

FIGURE 23.
The sodium retention was almost as pronounced as in the preceding patient but the potassium
loss was not so marked. The chief difference between the two patients was the condition of the wounds.
This patient had massive wounds but no residual nonviable tissue.

The peaks in the corticosteroid excretion on the fifth and tenth days were inversely related to the eosinophile count (Fig. 24). These peaks cannot be clearly associated with the operative trauma and would appear to be independent of any known insult. This patient was one of the casualties who demonstrated an increased excretion in 17-ketosteroids. Coincident studies of hepatic function demonstrated less hepatic impairment in this patient than in any seriously injured casualty studied. This maintenance of normal hepatic function may account for the high 17-ketosteroid excretion. Conn2 has suggested that the failure of the casualty to excrete an increased amount of 17-ketosteroids following severe trauma may be due to failure of the liver to form 17-ketosteroids from 17-hydroxysteroids. These changes, when compared with those of other casualties, again suggest the importance of necrotic tissue and infection in explaining the marked changes seen in other patients.

Patient No. 6. A 21-year-old American soldier, weight 175 lbs., blood type A, in Korea for 30 days, in combat 20 days.


58

FIGURE 24.
The patient had the most radical débridement, the healthiest wounds, the best hepatic function,
and the greatest excretion of 17-ketosteroids of any casualty studied. These findings may represent
additional evidence of the continuing effect of the wound on adrenal function.

This soldier was wounded by multiple shell fragments at 0330 hours, 3 August 1952. Arriving at the battalion aid station 1 hour later, he was given 15 mg. of morphine, 600,000 units of penicillin, and 0.5 cc. of tetanus toxoid. On arrival at the hospital at 0810 hours, his blood pressure was 148/78 and his pulse rate 104 per minute. He was pale and was considered to be in incipient shock. After 1,500 cc. of blood in the preoperative ward, his pressure was 160/100.

His wounds included a perforation of the right side of the chest, diaphragm and liver. The wound of the right lobe of the liver would easily admit four fingers. In addition, he had multiple small penetrating wounds of three extremities.

A laparotomy was performed and the hepatic wound was drained. Soft tissue wounds were débrided. Ether, oxygen and nitrous oxide were given by inhalation. His operative course was smooth, his pressure ranging about 120/75, his pulse rate 120. Another pint of blood was given during operation. Blood loss was estimated at 500 cc. during operation. Repeated thoracenteses were performed postoperatively until on the fifth day a tube drainage of the right side of the chest was elected.

Of the blood administered, 1 pint was freshly drawn, type-specific, and 3 pints were type O, bank blood, 12 days of age.

Discussion. The excretion of corticosteroids did not reach its peak until the second day after injury. It then fell to normal (Fig 25).  Again, after a


59

FIGURE 25.
The day of injury represents a period of 20 hours. The corticosteroid excretion
did not reach its peak until the second day after injury.  

minor secondary operation on the fifth day, the corticosteroid excretion showed a delayed increase. His 17-ketosteroid excretion was quite low, a circumstance due perhaps to direct hepatic injury.

The patient had a minimum sodium intake so that at the end of 11 days sodium retention was more apparent than at any previous time (Fig. 26). His plasma sodium concentration fell to 128 mEq./liter on the day after injury and then gradually returned to normal by the ninth day. His plasma potassium concentration rose from 3.8 mEq./liter postoperatively to 4.9 mEq./liter on the second day.

By comparison with the previous patients, this patient had minimal tissue destruction.

Patient No. 7. A South Korean soldier, approximately 25 years of age, blood type A.

This soldier was wounded by mortar shell fragments at 1130 hours, 20 September 1952. One hour later at the battalion aid station he was given penicillin and streptomycin. He arrived at the forward hospital at 1430 hours, at which time his blood pressure and pulse were imperceptible. He was lethargic: his skin was dry, and his capillary refilling was slow.

His wounds included a traumatic amputation of the left leg at the knee, four perforations of the ileum, one perforation each of the colon, liver and lung, a perforation of the right superficial femoral artery, and numerous penetrations of the extremities.

After 10 pints of blood, his pressure rose to 68/40, pulse rate 108 per minute. Operation was then started (1630 hours) under pentothal, nitrous oxide, oxygen, ether and curare anesthesia. Operation consisted of re-amputa-


60

FIGURE 26.
Because of the low sodium intake,
sodium retention only became apparent after 11 days.

tion of the left leg, repair of the right femoral artery, repair of the small bowel, and colostomy. The operation required 3 hours, and by the time of its completion he had received a total of 30 pints of blood.

His pressure ranged 90/60 to 70/40 until the last hour when his pressure became unobtainable, his pulse rate 60 per minute and quite irregular. Following operation his pulse spontaneously became regular at 110 per minute and his pressure rose to 120/80. At 2400 hours his pressure fell to 78/64, pulse 120. During the next 24 hours he was given 2,000 cc. of blood (total 34 pints type O, bank blood, 10 to 17 days of age), and his pressure slowly returned to 120/60, pulse rate falling from 120 to 105.

His subsequent convalescence was slow and marked by a febrile response (100°-102°) and a moderate paralytic ileus. His wounds were dressed on the fifth postoperative day, without anesthesia, and appeared clean.

Discussion. This patient had an abdominal wound followed by gastric suction. His corticosteroid excretion was quite high on the day after injury (Fig. 27). His potassium loss was marked and was followed by potassium retention (Fig. 28).

This patient had an injury comparable in magnitude to Patient No. 3. The differences in their adrenal and electrolytic responses were probably due to the conditions of their wounds. This patient retained no obviously gangrenous


61

FIGURE 27.
The first day, in this chart, is the day of injury and represents a period of only 8 hours.
The corticosteroid excretion the next day was extremely high.
The 17-ketosteroid excretion remained within normal limits.

tissue. Patient No. 3 retained a gangrenous limb. It appears that the body not only separates dead tissue as a slough but that it also has a mechanism which might be termed "metabolic débridement" by which products of tissue degeneration are absorbed, metabolized, or excreted.

Patient No. 8. A 30-year-old South Korean soldier, blood type B.

This soldier was wounded by mortar shell fragments at 1100 hours on 20 September 1952. The injuries included traumatic amputation of all four extremities; one leg at the calf, one leg at the knee, and both upper extremities at the forearm.  He was seen shortly thereafter at the battalion aid station where he was given albumin 500 cc., morphine 30 mg., streptomycin 1.0 gm. and penicillin 600,000 units.

He arrived at the hospital at 1330 hours. At this time his blood pressure could not be measured because of the drainage to all four extremities. His pulse rate was 102 per minute, and he was pale, lethargic and dry. No peripheral vessels were visible.

He was given 18 pints of blood intra-arterially. Meanwhile, hemostasis was obtained. The pulse rate averaged 130 to 140 per minute and was irregular.

At 2000 hours, under pentothal, oxygen and ether anesthesia, four surgical teams re-amputated all four extremities. The operation required only 20 minutes but was poorly tolerated. By the end of surgery, he had received 23 pints of blood (type O, 11 to 17 days of age) in addition to 5 units of albumin. The following day he received 3 more pints of blood. His subsequent convalescence was fairly slow but uneventful.


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FIGURE 28.
The potassium loss within 8 hours after beginning the study was tremendous.
This loss was proportionate to the magnitude of the injury and the amount of tissue destroyed.

FIGURE 29.
The corticosteroid excretion returned to normal on the fourth and fifth days
after injury, but on the sixth day, after a secondary dressing, it again increased.


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FIGURE 30.
Sodium retention persisted until the tenth day. Potassium loss was
quite marked for 2 days after which there was a period of relative
potassium balance and finally a period of potassium retention.

His wounds were dressed on the sixth postoperative day without anesthesia and appeared clean.

Discussion. Studies of the corticosteroid excretion demonstrated an elevation on the first day after injury and a gradual return to normal by the fourth and fifth days (Fig. 29). On the sixth day, following a secondary dressing of his extensive wounds, without anesthesia, the corticosteroid excretion showed a secondary rise. Again in this patient the 17-ketosteroid excretion remained normal throughout the period of study.

Sodium retention persisted until the tenth day (Fig. 30). Potassium loss was marked for 2 days and was followed by a conservation of potassium. At the end of 10 days he remained in a state of negative potassium balance (cumulative) (Fig. 31).

Patient No. 9. A 21-year-old American soldier, 170 lbs., blood type A, in Korea 3 months, in combat 4 hours.

This soldier was wounded at 0800 hours, 6 September 1952, by fragments from a mortar shell. His wounds included a traumatic amputation of the left leg at the knee, traumatic amputation of the right leg at the calf, two avulsive wounds of the right leg just distal to the knee and two of the buttocks. He arrived at the battalion aid station via litter at 1000 hours. Here he was given 200 cc. albumin and the dangling left leg was removed. A tourniquet was not used.

He arrived at the hospital at 1100 hours. His blood pressure and radial pulse were imperceptible. He was quite pale, cold and shivering. A tourniquet was applied to the left leg and blood was started intravenously and intra-arterially. Within 15 minutes he had received 2,500 cc. of blood and his pressure was 130/80.


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FIGURE 31.
Demonstrating the continued retention of sodium and
the initial loss and persistent deficit of potassium.

Operation was begun under pentothal, nitrous oxide, oxygen and ether at 1315 hours. His pressure gradually fell to 95/50, pulse rate 160 per minute. Revision of both amputations was performed, one at the mid thigh, the other at the calf. The wounds of the buttocks and knee were débrided. Operation was completed at 1450 hours after a total of 6,500 cc. of blood (type O, 11 days of age). His pressure at this time was 98/60, pulse rate 160.

He was given 500 cc. of blood immediately after operation and his blood pressure returned to a normal level: 1,000 cc. of fresh blood was given on the sixth postoperative day.

A secondary dressing under intravenous morphine analgesia was performed on the third postoperative day. The wounds appeared clean. His subsequent course was fairly smooth.

Discussion. This casualty demonstrated a secondary increase in the excretion of corticosteroids on the fifth through the eighth day after injury (Fig. 32). This could hardly have been the result of secondary operative trauma. His oral temperature, having been elevated to 100°-102° daily, was subsiding toward normal at this time.

His eosinophile concentration demonstrated a marked rebound after the initial fall. This increase in the eosinophile count on the sixth day was not associated with a subnormal corticosteroid excretion.

Patient No. 10. A 23-year-old American soldier, weight 155 lbs., blood type O, in Korea 3 months, in combat 17 days.


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FIGURE 32.
There was a sustained, late increase in corticosteroid excretion.
The eosinophile concentration fell and then rose to 620 cells/cc. on
the sixth day in spite of a continued adrenal cortical response.

This soldier was wounded at 0200 hours, 23 September 1952, by artillery shell fragments. The wounds included a traumatic amputation of the right leg at the knee and a compound fracture of the left humerus.

Tourniquets were applied and he was transported by litter and jeep to the battalion aid station, arriving there at 0900 hours. He was given 100 cc. of albumin and 15 mg. of morphine at that time.

He arrived via helicopter at the hospital at 1230 hours. He was in severe shock, was cold and shivering, with a grayish-cyanotic appearance. In addition, he was thirsty and his capillary refilling was slow. His blood pressure and peripheral pulses were imperceptible.

After 2,000 cc. of blood had been given intravenously under pressure, his blood pressure had risen to 150/112, pulse rate 80 per minute. In spite of continued transfusion, however, the pressure gradually fell to 118/80, pulse rate 85.

After 5,000 cc. of blood, operation was begun at 1600 hours under pentothal and ether anesthesia. A mild hypotension, 100/60, was corrected with 5.0 mg. of neosynephrine. A second drop from 130/70 to 90/60 occurred when, during re-amputation of the leg, the bone was divided. Débridement, casting and re-amputation were completed at 1740 hours. A total of 6,000 cc. of blood (type O, 10 to 19 days of age) had been given by this time.

Postoperatively his pressure rose spontaneously to 190/110, pulse rate 110, respiratory rate 24. The pressure then gradually fell toward normal.

His subsequent course was smooth.


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FIGURE 33.
Demonstrating the late peak in corticosteroid excretion.

Discussion. Again the corticosteroid excretion reached its peak on the second day after injury (Fig. 33). The amount excreted on the day after injury was less than half that excreted by the previous patient.

Patient No. 11. This 20-year-old American soldier, weight 178 lbs., was wounded at 0815 hours, 15 August 1952. The injury, inflicted by a land mine, consisted of a traumatic amputation of the right foot and multiple soft tissue wounds of the left thigh and leg. A tourniquet was applied immediately, and he was given 15 mg. of morphine.

On arrival at the hospital at 0955 hours, his blood pressure was 120/76, pulse rate 76, hematocrit 41 per cent. His skin was cool, dry, and pale, but his capillary refilling was rapid.

After 1,000 cc. of dextran his blood pressure was 148/82, pulse 84. Operation was then begun (1118 hours) under pentothal, nitrous oxide, oxygen and ether. With induction, his pressure dropped immediately to 104/38, pulse 104 per minute. Bleeding was rather rapid during the amputation, and his pressure dropped momentarily to 65/35, pulse rate 132 per minute. The pressure was partially restored by neosynephrine. At this time (1224 hours) he had received 2,500 cc. of dextran and his hematocrit was 20 per cent. Further hemodilution was considered unwise. Fresh drawn, type-specific blood was then given (1,000 cc.). Operation ended at 1256 hours, at which time his blood presure was 96/48, pulse rate 132. Another 500 cc. of fresh blood was given. His subsequent course was smooth until a hemolytic transfusion reaction on the fourth postoperative day resulted in a transient oliguria.

Discussion. This patient had an injury of a lesser magnitude than most of the others studied. His electrolyte and eosinophile responses were typical of a normal adrenal response (Figs. 34, 35). Because of the presence of dextran in


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FIGURE 34.
The eosinophile counts failed to demonstrate any persistent
drop after the secondary trauma of a hemolytic transfusion reaction.

the urine, corticosteroid analyses could not be performed. His 17-ketosteroid excretion was not elevated (Fig. 34). His plasma sodium and potassium concentrations demonstrated the inverse changes often seen on the first day after injury (Fig. 36). The transfusion reaction was severe enough to drop his urine volume from 2,500 cc. on the previous day to 250 cc. on the day of reaction. The eosinophile count, however, continued its rebound trend. If this secondary trauma produced any secondary decrease in eosinophile circulation, the depression was of short duration and not apparent the following morning.

Patient No. 12. A 22-year-old American soldier, weight 173 lbs., blood type A, in Korea 8 months, in combat for past 8 days.

This soldier was wounded at 1130 hours, 12 August 1952, by mortar shell fragments. He was given 100 cc. of albumin after which he was evacuated to the hospital via helicopter. He arrived at the hospital 1 hour after injury. At this time his blood pressure was 120/78. He was warm, pale, dry, with a fair capillary refill.

His wounds included partial amputation of the left foot and approximately 50 small penetrating wounds of both lower extremities.

The foot was amputated and many of the wounds débrided under spinal anesthesia. Operation, 1425 to 1540 hours, was associated with a drop in pressure with the onset of anesthesia. This was controlled by an intravenous drip of neosynephrine and by rapid administration of dextran. Blood loss from the operative wounds was approximately 2,000 cc.

By the end of operation, 3,400 cc. of dextran had been administered. The hematocrit had fallen to 12 per cent. A total of 3,000 cc. of fresh, type-specific


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FIGURE 35.
Demonstrating the moderate retention of
sodium and loss of potassium after trauma.

FIGURE 36.
Demonstrating the inverse changes in plasma potassium
and sodium concentrations which often occur following injury.


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FIGURE 37.
The sodium intake on the day of injury represents a net
intake over that lost by hemorrhage after the beginning of the study.

blood was then administered immediately postoperatively. His further course was marked by fever and slight necrosis of the edges of the amputation stump. Secondary débridement was carried out on the fifth postoperative day under spinal anesthesia. Repeated transfusions of fresh, type-specific blood were given. In spite of a rising hematocrit and blood volume, his pallor remained quite marked.

Discussion. This patient had only moderate trauma and was supported primarily with dextran. His sodium intake was tremendous. Nevertheless, his sodium retention was much less than in many of the more seriously injured men (Figs. 37, 38), The secondary trauma was minimal in degree. Again because of dextran in the urine, corticosteroid analyses could not be performed. The 17-ketosteroid excretion revealed an early, slight elevation (Fig. 39). His eosinophile count demonstrated a rebound to 570 and then only a slight and transient fall after secondary operation (Fig. 39).

Patient No. 13. This 24-year-old American soldier was wounded at 1430 hours, 28 July 1952, by small arms fire. He received 2,500 cc. of albumin at the battalion aid station and 100 cc. of albumin and 500 cc. of plasma at the collecting station. Prior to transfusion at the collecting station his blood pressure was 80/60.

On arrival at the hospital at 1830 hours, his blood pressure was 130/70, pulse rate 130 per minute. After 1,500 cc. of blood, laparotomy was begun. His blood pressure fell and remained unobtainable for 45 minutes. Approximately 1,500 cc. of blood was found in the peritoneal cavity. The vena cava was found perforated distal to the renal veins. Ligation at this point was performed. A perforation of the duodenum was closed. Operation required 2 hours and was performed under pentothal, ether and curare. An additional 18 pints of blood (total 21 pints, type O, 18 days of age) was given during operation. His pressure never rose over 90/60 and his pulse rate never fell below 130 per minute.


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FIGURE 38.
The sodium and potassium balances remained fairly stable after the first few days.
Secondary trauma was followed by a secondary, transient retention of sodium.
The specimen on the seventh day was not analyzed.

Postoperatively his pressure gradually rose to 136/110, pulse rate 120. The pressure then slowly fell to 120/90, pulse 90, and both stabilized at this level for 48 hours.

He was evacuated on the fourth postoperative day because of post-traumatic oliguria with azotemia.

Discussion. This patient had an injury so severe that he developed post-traumatic renal insufficiency. Although his eosinophile count showed a transient drop (Fig. 40), and he selectively conserved sodium (Fig. 41), he did not demonstrate a rise in steroid excretion (Fig. 40). It is probable that this was due to inadequate renal function rather than to adrenal insufficiency. Plasma steroid determinations might demonstrate an elevated concentration under these circumstances. It is of interest that in this early period, his renal tubules could conserve sodium and excrete potassium.

Patient No. 14. This 22-year-old American soldier, blood type A, was wounded at 1115 hours, 12 August 1952, by mortar fragments. The wounds included an incomplete traumatic amputation of both legs at the calf.


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FIGURE 39.
The 17-ketosteroid excretion was increased on the second day.
The eosinophile concentration diminished slightly after secondary trauma.

At the battalion aid station, 1145 hours, he was given 400 cc. of albumin. On arrival at the hospital at 1254 hours via helicopter he appeared in a critical condition, but he responded well to transfusion. After 2000 cc. of blood his pressure was 120/65, pulse rate 120 per minute.

After 10 pints of blood débridement was begun under pentothal, nitrous oxide, oxygen and ether. Another pint of blood along with neosynephrine was used during operation. Postoperatively he was given another 1,000 cc. of blood (total of 13 pints, type O, 11 days of age).

His postoperative course was marked by the development of gas gangrene in both legs and by a transient post-traumatic oliguria. He almost died on the third postoperative day of toxemia but responded well after amputation and dialysis on an artificial kidney.

Discussion. This patient had a wound of which he very nearly died. Study was discontinued on the third day post-injury as he was evacuated because of post-traumatic oliguria. A rather clear-cut adrenal response is depicted in spite of these complications (Fig. 42). He too selectively conserved sodium and excreted potassium during the early development of post-traumatic renal insufficiency (Fig. 43). In the presence of a normal urinary output, he would doubtless


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FIGURE 40.
Post-traumatic renal insufficiency evidently resulted in a retention of the steroids.

FIGURE 41.
Post-traumatic renal insufficiency in this early stage and moderate degree
was associated with renal retention of sodium and excretion of potassium.


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FIGURE 42.
The continued eosinophile depression was to have been expected in this patient,
but the fall in corticosteroid excretion on the day after injury is probably the result of the renal failure.

FIGURE 43.
The patient continued to excrete more potassium than sodium in his urine,
indicating the relative maintenance of this tubular function. Part of his electrolyte loss
included in the two upper charts resulted from loss of gastric fluids.


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FIGURE 44.
The corticosteroid excretion did not reach its maximum until the
second day after injury. The 17-ketosteroid excretion was slightly increased.

have excreted much more potassium. His plasma sodium concentration fell to 120 mEq./liter on the day after injury, and his plasma potassium concentration gradually rose to 6.2 mEq./liter by the third day.

Patient No. 15. An 18-year-old American soldier, weight 170 lbs., blood type A, in Korea 11 months, in combat area 9 months.

This soldier was wounded at 0845 hours, 2 September 1952, by the discharge of a burp gun at close range. Immediately thereafter, 0900 hours, at the battalion aid station, he was given l00 cc. of albumin, 500 cc. of plasma and 15 mg. of morphine.

He arrived via helicopter at the hospital at 1010 hours with a blood pressure of 200/66, and 1,000 cc. of blood was given preoperatively. Laparotomy was then performed under pentothal, nitrous oxide, oxygen and ether. Perforation of the internal iliac artery and vein as well as perforation of the colon was found, and 3,600 cc. of blood was aspirated from the abdominal cavity. The vessels were ligated and a colostomy was performed. During operation, 5,000 cc. of blood was given. Operation required 4 hours and was uneventful. An additional l,000 cc. of blood was given postoperatively (total 7,000 cc., type O, 11 days of age).

This patient's blood pressure ranged around 140/70, pulse rate 100 to 120, respiratory rate 36 to 48 during the succeeding 12 hours. His subsequent improvement was slow and marked by the development of a transient jaundice and a febrile course. An additional 2,000 cc. of blood was given during convalescence.

Discussion. This casualty was one of the few who demonstrated a slight, early rise in 17-ketosteroid excretion. His excretion of corticosteroids was very high for 2 days, after which it fell to normal (Fig. 44). His eosinophile count never


75

FIGURE 45.
The electrolyte studies were not begun before operation so that the earliest changes
are not recorded. The trauma of opening the colostomy without anesthesia
apparently produced a fall in plasma sodium concentration.

rose over 156 and fell to zero on the eleventh day without any coincident operative trauma other than the re-opening of his colostomy, without anesthesia or discomfort, on the preceding day (Fig. 44). His plasma sodium and potassium concentrations likewise revealed slight inverse changes on this day (Fig. 45).

Patient No. 16. This 20-year-old American soldier, blood type B, was wounded at 1300 hours, 3 September 1952, by the discharge of a carbine at close quarters. The bullet perforated the liver, stomach, transverse colon, diaphragm and left lung.

At the battalion aid station he was given 100 cc. of albumin, 600,000 units of penicillin, and tetanus toxoid. At 1420 hours, he was given 500 cc. of blood at the collecting station.

When he arrived at the hospital at 1840 hours, his blood pressure was unobtainable. He was pale, dry and very quiet. His pulse was barely perceptible at the wrist. His veins were not visible and capillary refilling was slow.

After receiving 1,500 cc. of blood in 15 minutes, his pressure was 90/40. After 3,000 cc. of blood, part intra-arterially, his pressure was 125/175. As did many other patients, he complained of cold and shook the litter by shivering.

Operation was started at 1940 hours. His pressure was 170/80, pulse rate 125. After 3,500 cc. of blood had been given at the hospital, operation was begun under pentothal (300 mg. total), ether, oxygen, curare (80 units total). His pressure gradually dropped to 90/50, pulse rate 140 per minute.

Operation revealed 300 cc. of blood in the peritoneal cavity. Another 500 cc. was removed during the course of the operation. Finally, 1,000 cc. was removed from the left pleural cavity. Operation consisted of drainage of the liver, colostomy and closure of the gastric wounds. The pleural cavity was aspirated and the wounds of entrance and exit débrided. An additional 2,000 cc. of blood (6,000 cc. total, type O, 12 days of age) was given during operation. His pressure ranged between 90/60 and 105/60 most of the 2 hours required for operation.

His postoperative course was marked by hemoconcentration with an hematocrit reaching 63 per cent for a few hours. His oral temperature ranged between 101° and 103° because of wound infections.


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FIGURE 46.
Seventeen-ketosteroid excretion was increased on the day of injury in spite of an
hepatic wound. Corticosteroid excretion remained high as a result of the continued trauma of infection
and the repeated trauma of thoracentesis. The eosinophile concentration was quite slow to rise.

Discussion. This casualty demonstrates the continued adrenal response to the continued trauma of infected wounds, and the repeated traumas of thoracentesis. He remained febrile throughout the 12 days of study. His corticosteroid excretion remained high for most of his hospital course. His eosinophile count was slow to rise (Fig. 46). Again, he demonstrates minor changes in plasma sodium and potassium concentrations after the secondary minor injuries of repeated thoracentesis under local anesthesia (Fig. 47).

Summary

The Noncombat Soldier

1. The eosinophile count was performed daily for 2 or 3 days on 11 soldiers in a noncombat area. The mean count was 142 with a standard deviation of 67.

2. The average daily excretion of 17-ketosteroids was 13.6 mg. with a range of 9.9 to 21.9 mg. The normal range for the method used is 8.0 to 22.0 mg.

3. The average daily excretion of corticosteroids (formaldehydogenic compounds) was 2.0 mg. with a range of 0.9 to 4.4 mg. The normal range for the method used is 0.6 to 2.6 mg.


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FIGURE 47.
Repeated injuries apparently produced repeated, small, inverse
changes in plasma sodium and potassium concentrations.

The Front Line Soldier

1. The eosinophile count of the front line soldier was normal.

2. The 24-hour excretion of 17-ketosteroids was normal.

3. The 24-hour excretion of corticosteroids was normal or increased.

The elevation in excretion could not always be correlated with the combat activity.

The Immediate Response to Injury

1. Minimal injuries usually, but not always, resulted in a fall in the eosinophile count.

2. There appeared to be a threshold trauma necessary to produce a fall in the concentration of the circulatory eosinophiles.

3. The threshold having been reached, a drop in eosinophile count was invariable.

4. In this series, including six men with massive, fatal or near fatal wounds, there was no indication of an inadequate adrenal response as measured by the immediate drop in the eosinophile count.

Studies During Early Convalescence

1. In these severely injured patients the eosinophile concentration, having dropped with the initial injury, remained low for several days. It then tended to rise above normal for 1 to 3 days before returning to a normal level.


78

2. Following injury there was a marked increase in the excretion of the corticosteroids (formaldehydogenic compounds) which reached a peak on the first or second day after injury. There was a characteristic decrease in excretion on the third to the fifth day post-injury. Following this drop there was sometimes a secondary rise. Secondary trauma after the third day was characteristically followed by a rise in excretion. The excretion of corticosteroids was usually inversely proportional to the eosinophile concentration.

3. Following injury, the excretion of the 17-ketosteroid fraction seldom exceeded normal limits.

4. The casualty conserved sodium and excreted potassium for several days after injury. Thereafter this balance was usually reversed. However, with repeated injuries (débridement, anesthesia) the continued sodium conservation and potassium loss was prolonged and reached very high proportions.

5. The presence of gangrenous or infected tissue was associated with a prolonged stress response.

Recommendations for Further Study

1. Adrenal function in combat fatigue.

2. Adrenal function in post-traumatic renal insufficiency. Plasma steroid levels should, if feasible, be determined in the anuric patients.

3. The significance of the decrease in plasma sodium concentration following injury.

Conclusions

Combat stress, under the conditions and limitations of this study, did not result in adrenal cortical insufficiency. An increased adrenal cortical function is often found in the combat soldier.

The study of the injured soldier is a study of repeated injury with repeated responses of the adrenal cortex.

Gangrenous or infected tissue is a major, continuing injury to which the adrenal cortex may continue to respond.

Acknowledgments

The authors wish to acknowledge the complete cooperation of the officers and men, wounded and unwounded, who participated in this study.

Appreciation is also extended for the assistance of Captains John H. Davis, MC, Lloyd H. Smith, MC, Roy L. Mundy, MSC, Paul Teschan, MC, Lieutenant Russell Scott, Jr., MC, Lt. Colonel George Hayes, MC, and Dr. Fred Elmadjian, in the various phases of this


79

study in Korea; and to Colonel William S. Stone, MC,Colonel Richard Mason, MC, and Lt. Colonel Monroe Freeman, MSC, for their assistance in the Army Medical Graduate School and the 406th Medical General Laboratory.

Finally, the authors wish to acknowledge the assistance of Dr. Francis D. Moore in developing the balance studies of sodium and potassium. His method of charting the balance studies5 has been used throughout this report.

References

1. Cahen, R. L., and Salter, W. T.: Urinary 17-Ketosteroids in Metabolism. J. Biol. Chem. 152: 489-499, 1944.

2. Conn, J. W.: Discussion before the Committee on Metabolic Response to Trauma, Army Medical Service Graduate School, 4 November 1953.

3. Daughaday, W. H., Jaffe, H., and Williams, R. H.: Chemical Assays for "Cortin." J. Clin. Endocr. 8: 166-174, 1948.

4. Ladd, M.: Renal Function in the Combat Casualty, Report to the Army Medical Service Graduate School, 1952.

5. Moore, F. D., and Ball, M. R.: The Metabolic Response to Surgery. Charles C. Thomas, Springfield, Illinois, 1952.

6. Renold, D. E., Jenkins, D., Forsham, P. H., and Thorn, G. W.: The Use of I. V. ACTH: A Study in Quantitative Adrenocortical Stimulation. J. Clin. Endocr. and Metab. 12: 763, 1952.

7. Wright, A., Baker, J. W., Merrington, W. R., and Cope O.: The Ebb and Flow of the Eosinophils in the Burned Patient and Their Use in the Clinical Management. Ann. Surg. 137: 175-183, 1953.

8. Zimmerman, W. Z.: Physiol. Chem. 233: 257, 1935.

9. Zimmerman, W. Z.: Physiol. Chem. 245: 47, 1936.