U.S. Army Medical Department, Office of Medical History
Skip Navigation, go to content

HISTORY OF THE OFFICE OF MEDICAL HISTORY

AMEDD BIOGRAPHIES

AMEDD CORPS HISTORY

BOOKS AND DOCUMENTS

HISTORICAL ART WORK & IMAGES

MEDICAL MEMOIRS

AMEDD MEDAL OF HONOR RECIPIENTS External Link, Opens in New Window

ORGANIZATIONAL HISTORIES

THE SURGEONS GENERAL

ANNUAL REPORTS OF THE SURGEON GENERAL

AMEDD UNIT PATCHES AND LINEAGE

THE AMEDD HISTORIAN NEWSLETTER

Chapter VIII

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

Hepatic Function of the Battle Casualty*

First Lieutenant Russell Scott, Jr., MC, USAR
First Lieutenant John M. Olney, MC, USAR
Captain John M. Howard, MC, USAR

This study of hepatic function of the battle casualty was part of a broad survey of the systemic response to injury carried out by the Surgical Research Team of the United States Army in Korea during 1952-53. As in the study of other systems, the results of this phase of the study indicate gross alteration in the physiology of the wounded man. This response to injury is not a response of a few hours but one of days or weeks in duration. Even though a particular system may not be directly damaged by the initial trauma, reflex vascular changes, anoxia, toxins or hormonal influence may simultaneously affect the function of an organ or system. A bullet through the thigh does not injure only the thigh, it injures the entire individual. It is, therefore, not surprising that the individual in his entirety responds to the injury.

It would be desirable to interpret hepatic response in terms of vital functions, such as the production of energy, prothrombin, albumin, fibrinogen, cholinesterase, the metabolism of hemoglobin, citrate, morphine, pentothal and other drugs; the stability of the ferratin hemostatic mechanism (VDM and VEM), the detoxification of bacterial toxins and the many other functions so vital to the critically injured man.

The present study does not permit a complete interpretation of hepatic response in terms of vital function. It only permits a view of hepatic response in the wounded man based on observations which could be made in a forward combat area.

This study was performed during the summer of 1952 and the winter of 1952-53 at a forward Surgical Hospital in Korea. The casualties usually arrived at the hospital between 3 and 5 hours after wounding with range of 1 to 9 hours. The soldiers were all young and previously healthy. As a generalization, the more severely injured men were selected for study. Shortly after injury, the casualty was treated at the battalion aid station. When needed, plasma, albumin or dextran was administered along with tetanus toxoid and penicillin. The 


*An abbreviated version of this article is currently being published in Surgery, Gynecology and Obstetrics.


150

casualty was then evacuated to the forward Surgical Hospital for definitive therapy where this study was begun. A series of hepatic function tests were then performed during the period of transfusion, operation, and the first 5 to 14 days of convalescence. Detailed clinical records were maintained throughout the period of study. Blood, 10 to 20 days of age, was used almost exclusively after the casualty reached the hospital. Operations were performed under pentothal, nitrous oxide, oxygen and ether anesthesia.

Observations made on the Korean battle casualty demonstrate a rise in plasma hemoglobin and bilirubin after injury and transfusion, an increase in the ulinary excretion of urobilinogen, an abnormal bromsulphalein retention, a positive cephalin flocculation reaction, a normal thymol turbidity, a fall in prothrombin activity, a rapid production of fibrinogen2 and albumin,34 an increase in blood glucose concentration,31 a resistance to insulin,31 a maintenance of an essentially normal plasma cholinesterase concentration,33 and the release of ferratin into the circulation.

Results

Plasma Bilirubin

The plasma bilirubin concentration was studied in 15 normal soldiers and 25 seriously injured soldiers. Following injury, the plasma bilirubin concentration was characteristically normal on admission, became elevated during resuscitation and followed a variable pattern thereafter.

The plasma bilirubin concentration in the unwounded soldier averaged 0.3 mg. per 100 ml. with a range of 0.1 to 0.7 mg. per 100 ml. Thirteen casualties were studied on admission to the hospital prior to having received blood transfusion (Table 1). The plasma bilirubin concentration was normal (average 0.4 mg. per 100 ml. in the 12 patients studied 1 to 5 hours after injury, but was high (1.2 mg. per 100 ml.) in the one patient (Table 1, Patient 39) who reached the hospital 9 hours after injury. Following transfusion, but before operation, the plasma bilirubin was found to be consistently elevated (15 patients). This group of 15 casualties had received 500 to 6,500 ml. of blood preoperatively (average 2,500 ml.), and their preoperative bilirubin values ranged from 0.4 to 4.9 mg. per 100 ml. (average 1.6 mg. per 100 ml.). The elevation was due to an increase in the indirect component as measured by the van den Bergh reaction. None of the direct values had increased above 0.3 mg. per 100 ml. prior to anesthesia and operation.

Postoperatively, the bilirubin remained elevated for at least 12 hours. It averaged 1.8 mg. per 100 ml. immediately after surgery


Table 1. Plasma Bilirubin Data Sheet
(See footnotes at end of table) ;

Patient Number

Injury

Shock and Points

Total ml. Therapy Before Admission

Admission Bilirubin

Total ml. Therapy
Before Operation

Preop. Bilirubin

Operative Procedure

Total ml. Therapy by End of Operation

Plasma Bilirubin

Albumin

Plasma

Blood

Albumin

Plasma

Blood

Albumin

Plasma

Blood

Hours Postoperative

Days Postoperative

0

6

12

24

2

3

4

5

6

7

8

9

10

1

MPW, legs, small intestine, bladder

Mod. 5.4

100

---

---

---

100

---

1,000

---

Debridement, repair

100

---

1,000

---

---

.8/1.8

---

.3/.7

.3/.6

.2/.5

.5/.7

.4/.6

---

---

---

---

2

MPW, small intestine, laceration of vena cava

Mod. 10.0

100

500

---

---

100

50

8,000

---

Repair

100

500

10,000

2.0

.3/2.5

---

---

1.5/3.4

.2/1.1

---

---

---

---

---

---

---

3

MPW, small intestine, legs, laceration of vena cava

Severe 12.5

200

---

---

---

200

---

5,000

---

Repair

200

---

10,500

.7/.6

.5/8

---

---

.5

.7

.1/1.6

.1/1.0

.9

.2/1.2

.2/.8

.2/.7

.1/.6

4

MPW, chest, diaphragm, liver

None 8.4

---

---

---

---

---

---

500

---

Debridement, repair

---

---

1,500

---

---

---

.3/1.1

.8

.7

.1/.3

.2/.1

.4

.1/.3

.1/.2

.1/0

---

5

MPW, small intestine, large retroperitoneal hematoma

None 4.3

---

---

---

---

---

---

500

---

Repair

100

---

1,500

---

---

4.0

---

2.8

.1/.7

.2/.5

.6

.1/.5

.1/.3

.1/.4

---

---

6

Perforation of stomach

None 4.2

---

500

500

---

---

500

500

---

Repair

---

500

2,000

---

---

1.7

---

2.3

.1/.7

.1/.4

.3

.1/.2

.1/.2

.1/.6

0/.2

---

7

Perforation of diaphragm, liver

None 6.8

---

---

---

---

---

---

1,000

---

Repair

---

---

1,500

---

---

---

1.0

0/.6

0/.2

.4

.1/.3

.1/.1

---

---

---

---

8

MPW with fracture of tibia and radius

None 2.7

---

500

---

---

---

500

1,000

---

Debridement

---

500

1,000

---

---

1.4

---

0/.4

.1/.3

.2

.2/.2

0/.4

---

---

---

---

9

MPW, colon, kidney

None 5.3

100

---

500

---

100

---

1,000

---

Nephrectomy, repair of colon

100

---

1,500

---

---

.5

---

.1/.3

.2/.1

---

.2/.3

.2/.1

.2/.7

---

---

---

10

MPW, extensive, legs

Severe 8.5

---

---

---

---

---

---

3,000

---

Debridement

---

---

4,500

1.3

---

.2/1.4

---

.1/.4

---

---

---

---

---

---

---

---

11

MPW, fracture both femurs

Mod. 12.0

100

---

1,000

---

100

---

4,500

---

Debridement

100

---

9,500

.2/1.3

---

---

.3/2.1

.1/1.1

.2/1.1

---

.1/.8

0/.5

.4/1.1

.6/.9

1.1/1.9

---

14

MPW, legs, amputation of foot

None 5.5

100

---

---

0/.1

200 

Dextran 800

---

---

Surgical amputation, debridement

100

3,400
Dextran

---

0.2

0.1

---

---

0.2

---

---

0.5

1.1

0.6

---

0.5

---

15

MPW, shoulder

None 5.7

200

1,000

1,000

0.9

200

1,000

2,500

---

Debridement

200

1,000

3,000

2.5

---

---

2.7

.2/.6

.2/.1

.2/.1

.2/.1

---

.2/.4

---

---

---

21

Laceration, liver

Mod. 7.8

---

---

---

---

500

1,500

2,000

---

Repair of liver

500

1,500

4,000

---

---

---

---

1.9

1.2

---

1.3

1.2

2.0

6.6

6.4

---

22

MPW, arm, leg

None 5.7

200

---

---

0/.1

200

---

2,000

---

Debridement

200

---

3,000

1.0

---

---

0.7

.1/1.2

.1/.1

.1/.2

.2/.7

---

.1/.1

---

---

---

23

Bilateral traumatic amputation below knees

None 5.7

200

500

1,000

---

200

500

3,000

.3/.3

Surgical amputation

200

500

6,500

.6/.9

---

---

.5/3.6

.3/4

.2/.4

.2/.6

.1/.5

.2/.1

.2/.4

.2/.6

.2/.5

.1/.2

24

MPW, small intestine, ureter

Mod. 8.0

100

---

---

---

100

---

1,000

---

Repair, anastomosis of ureter

100

---

2,500

---

---

---

---

---

.3/.1

.1/.2

.3/.3

.5/.5

.4/.5

.2/.1

---

---

25

Traumatic amputation of foot

None 3.7

---

---

---

.2/.5

---

---

500

---

Surgical amputation

---

---

1,000

.4/1.7

---

---

.4/2.6

.1/.2

.2/.2

.1/.2

.2/.5

---

.2/.2

.2/.3

.2/.4

.2/.4

26

Bilateral traumatic amputation below knees

Mod. 10.6

---

---

1,500

---

---

---

6,000

---

Surgical amputation

---

---

9,500

.1/3.5

---

0/5.6

---

0/1.0

0/.8

0/.7

0/.9

0/.3

0/.5

0/.5

0/.5

0/.5

27

Laceration of iliac artery, colon

Mod. 5.1

100

500

---

---

100

500

3,500

---

Repair

100

500

6,000

---

---

.3/2.5

---

.6/2.7

1.4/2.5

.5/1.7

2.5/2.1

2.0/2.9

1.9/2.5

.4/1.4

.3/.6

.3/.6

28

MPW, liver, stomach, colon, diaphragm

Severe 10.2

100

---

500

---

100

---

5,000

---

Repair

100

---

5,500

---

---

.1/2.9

---

0/1.0

.1/.7

.1/1.5

.2/1.4

.2/1.1

.1/.7

.1/.5

.1/.3

---

29

MPW, legs, traumatic amputation of foot

Severe 8.5

200

---

---

0/.2

200

---

2,000

---

Debridement, surgical amputation

200

---

7,000

.5/2.5

---

---

.3/2.7

.1/.8

.1/.8

0/.6

---

---

0/.3

0/.3

---

---

30

Quadruple traumatic amputations

Mod. 11.9

500

---

---

---

500

---

9,000

---

Surgical amputation

500

---

11,000

1.1

---

1.2

---

0/.8

0/.5

---

0/.5

0/.7

---

0/.4

---

---

31

MPW with traumatic amputation of leg, perforation of large and small intestine

Severe 14.5

---

---

---

---

---

---

7,000

---

Surgical amputation, repair

---

---

15,000

.7

.6/2.4

.6/2.4

---

.1/1.5

.1/1.9

.1/2.6

.4/2.9

.4/3.2

.3/2.4

.1/2.3

.1/2.0

.2/2.2

32

MPW with traumatic amputation of leg

Mod. 9.0

100

---

---

---

100

---

3,500

1.8

Surgical amputation, repair

100

---

6,000

2.6

---

.9

---

0/.4

---

0/.4

---

---

---

---

---

---

33

MPW, chest, lung

Mod. 3.2

---

---

---

.2/.3

---

---

2,000

.3/1.8

Debridement under local anesthesia

---

---

2,000

.3/1.8

.1/2.1

.1/1.8

.1/1.0

.2/1.2

.2/.9

0/1.0

0/1.0

.1/1.2

.1/1.1

0/.7

0/.8

0/.8

34

MPW, arms, legs

Mod 5.7

---

---

500

.1/1.8

---

---

6,500

.1/4.8

Debridement 

---

---

7,500

.4/3.6

.1/4.2

.2/4.3

.2/2.6

.2/2.4

.2/1.4

.1/1.9

.1/.9

.2/1.0

.4/1.3

.2/.9

.1/.8

.1/.8

35

MPW, arms, legs

None 4.7

---

---

500

0/.5

---

---

1,500

.2/1.0

Surgical amputation, debridement

---

---

2,500

0/2.0

.2/3.6

.1/1.5

.1/.3

0/.8

.1/.7

0/.5

0/.4

0/.4

0/.5

---

---

---

36

MPW, arms, legs

Mod. 4.3

---

---

---

0/.5

---

---

1,200

.1/1.8

Debridement

---

---

2,000

1.1

.1/1.8

.1/1.4

1.2

.1/1.0

0/.8

0/1.1

.1/1.3

0/.8

0/.9

0/.8

0/.8

.1/.7

37

MPW, abdomen

None 3.3

---

250

---

0/.4

---

250

750

0/.4

Negative Exploration

---

250

1,500

.1/.8

---

.1/.6

0/.5

.1/.6

0/.5

.1/.8

0/.3

0/.4

0/.4

---

---

---

38

MPW, chest, back

Mod. 6.0

200

500

---

0/.3

200

500

1,300

0/1.2

Debridement and chest tap

200

500

3,000

---

---

0/3.0

1.8

---

---

---

---

---

---

---

---

---

39

Traumatic amputation of foot

None 5.7

---

500

---

.1/1.1

---

500

500

1.0

Surgical amputation

---

500

500

1.1

0.8

---

---

---

---

---

---

---

---

---

---

---

40

Bilateral traumatic amputation below knees

None 8.4

---

---

300

---

---

---

2,200

.1/1.9

Surgical amputation

---

---

4,250

.2/3.3

.1/3.3

---

---

---

---

---

---

---

---

---

---

---

41

MPW, back, fracture femur

Mod. 5.9

---

---

---

0/.1

---

---

1,000

.1/1.0

Debridement

---

---

3,500

0/.8

0.6

.1/.7

0/.6

 

 

 

 

 

 

 

 

 

42

MPW with perforation large and small intestine, arms, legs

Severe 13.3

600

1,500

---

.1/.5

600

1,500

4,500

.1/.4

Debridement and repair

600

1,500

14,000

.2/.7

Died

---

---

 

 

 

 

 

 

 

 

 

43

MPW, fracture tibia

Mod. 3.3

---

---

---

0/.4

---

---

1,000

0/1.8

Debridement

---

---

1,000

0/1.8

.2/3.2

1.8

.1/1.8

 

 

 

 

 

 

 

 

 

44

MPW, back

Mod. 3.9

---

---

---

0/.4

---

---

1,000

0/.3

Debridement

---

---

2,500

.1/.5

0/.5

0/.7

0/.7

 

 

 

 

 

 

 

 

 

45

Bilateral traumatic amputation below knees

Severe 12.0

200

500

3,000

0/.4

200

500

6,000

0/1.9

Surgical amputation

200

500

10,000

.2/2.3

0/2.6

.2/2.4

---

 

 

 

 

 

 

 

 

 

46

MPW, liver, small intestine, amputation below knee

Severe 14.0

200

---

---

0/.4

200

---

4,900

0/1.6

Died in operating room

---

---

---

---

---

---

---

 

 

 

 

 

 

 

 

 

Abbreviations and Symbols
State of Shock and Points--see Appendix
MPW--multiple penetrating wounds

Plasma Bilirubin Concentration is reported as the total concentration
or as the direct over the indirect component in milligrams per 100 milliliters
(normal 0.7 mg. per 100 ml. or less).


Table 2. Bromsulphalein Retention
(See footnotes at end of table.)

Patient Number

Injury

Shock and Points

Operation

Total ml. Treatment

BSP % Retention Days Postoperative

Albumin

Plasma

Blood

1

2

3

4

5

6

7

8

9

10

11

3

MPW, small intestine, legs, laceration of vena cava

Severe 12.5

Debridement, repair

200

---

10,500

27

---

11

---

---

21

---

---

7

---

---

4

MPW, chest, diaphragm, liver

None
8.4

Debridement, repair

---

---

---

19

---

14

---

---

24

---

---

---

19

---

5

MPW, small intestine, large retroperitoneal hematoma

None
4.3

Repair

100

---

1,500

16

11

10

---

---

---

---

8

---

---

---

6

Perforation of stomach

None 4.2

Repair

---

500

2,000

12

---

5

---

---

---

---

5

---

---

---

Perforation, diaphragm, liver

None 6.8

Repair

---

---

1,500

5

---

4

---

---

6

---

---

---

---

---

8

MPW with fracture of tibia and radius

None 2.7

Debridement

---

500

1,000

---

4

4

---

---

1

1

---

---

---

---

9

MPW, colon, kidney

None 5.3

Nephrectomy, repair of kidney

100

---

1,500

21

---

17

16

---

---

---

---

---

---

---

10

MPW, extensive legs

Severe 8.5

Debridement

---

---

4,500

25

---

---

---

---

---

---

---

---

---

---

11

MPW, fracture both femurs

Mod. 12.0

Debridement

100

---

9,500

19

---

11

---

---

---

---

---

---

---

---

16

MPW, extremity, perforation femoral artery

Severe 6.0

Debridement, anastomosis.

---

---

6,000

32

---

6

5

---

---

1

---

---

---

---

17

Perforation of stomach and small intestine

Mod. 7.0

Repair

---

---

6,500

29

---

10

---

---

5

4

---

---

---

---

18

MPW, chest, brachial artery

Severe
9.0

Debridement, anastomosis

---

1,000

4,500

42

---

17

---

---

20

---

---

---

---

---

19

Traumatic amputation above knee

Severe 6.5

Surgical amputation

100

---

4,000

13

---

---

---

---

---

---

---

---

---

---

20

Traumatic amputation above knee

Mod. 6.0

Surgical amputation

---

---

6,500

13

---

---

---

---

---

---

---

---

---

---

21

Laceration of liver

Mod. 7.8

Repair

---

---

4,000

25

---

8

---

---

---

---

---

---

---

---

26

Bilateral traumatic amputation below knee

Mod. 10.6

Surgical amputation

---

---

9,500

5

1

1

---

1

1

---

---

---

---

1

27

Laceration of iliac artery

Mod. 5.0

Repair

100

500

5,500

27

---

31

---

---

31

---

---

---

---

22

28

MPW, liver, stomach, colon, diaphragm

Severe 10.2

Repair

100

---

5,500

21

---

22

---

---

---

---

21

---

---

---

29

MPW, legs, traumatic amputation of foot

Severe 8.5

Debridement, surgical amputation

200

---

7,000

18

---

---

9

---

---

---

---

---

---

15

30

Quadruple traumatic amputations

Mod. 11.9

Surgical amputations

500

---

11,000

4

---

6

---

---

---

---

---

---

---

---

31

MPW with traumatic amputation of leg, perforations of large and small intestine

Severe 14.5

Surgical amputation, repair

---

---

15,000

40

---

14

---

---

---

---

---

---

---

---

34

MPW, arms, legs

Mod. 5.7

Debridement

---

---

7,500

3

---

---

---

---

---

---

---

---

---

---

37

MPW, abdomen

None 3.3

Negative exploration

---

250

1,500

12

---

---

---

---

---

---

---

---

---

---

Abbreviations and Symbols
State of Shock and Points--see Appendix
MPW--multiple penetrating wounds
 

Bromsulphalein Retention is reported as the per cent dye retention 45 minutes
after the intravenous injection of 5 mg. of dye per kg. of body weight
(normal 7 per cent retention or less).


Table 3. Urine Urobilinogen and Plasma Bilirubin
 

Patient Number

Injury

Shock Points

Operation

Total ml. Therapy

Study

Postoperative Day

Albumin

Plasma

Blood

1

2

3

4

5

6

7

8

9

10

11

MPW, fracture both femurs

Mod.
12.0

Debridement

100

---

9,500

Urobil.
Bil.

8.5 2.4 

46.2 1.1 

6.8 1.3 

7.7
--- 

21.5 0.9 

35.4 0.5 

82.8 1.5 

50.4 1.5 

14.5 3.0 

---
---

26

Bilateral traumatic amputations below knee

Mod. 10.6

Surgical amputations

---

---

9,500

Urobil.
Bil.

26.7 5.6

11.0 1.0 

2.0 0.8

21.0 0.6

34.0 0.9

1.0 0.3 

1.4 0.5

0.4 0.5

7.6 0.5

0.8
---

27

Laceration of iliac artery, colon

Mod. 5.1

Repair

100

500

6,000

Urobil.
Bil.

2.4 2.8

3.1 3.3 

13.0 3.9

125.0 2.2

224.0 4.6

29.0 4.9

36.0 4.4

25.0 1.6

2.0 0.9

4.0 0.9

28 

MPW, liver, stomach, colon diaphragm

Severe 10.2

Repair

100

---

5,500

Urobil.
Bil.

1.0 3.0

2.0 1.0 

0.8 1.8

2.0
1.6

6.9 
1.6

1.4 1.3

0.4 0.8

0.9 
---

0.9 0.4

0.6 
---

29

MPW, legs, traumatic amputation of foot

Severe 8.5

Debridement, surgical amp.

200

---

7,000

Urobil.
Bil.

15.0 3.0

11.0 0.9

11.0 0.9

21.0 0.6

37.0 
---

52.0
---

78.0 0.3

40.0 0.3

45.0 
---

---
---

30

Quadruple traumatic amputations

Mod. 11.9

Surgical amputations

500

---

11,000

Urobil.
Bil.

3.0 1.2

13.7 0.8

30.6 0.5

5.1 
---

34.0 0.5

11.0 0.7

12.9 
---

0.9 0.4

2.9
--- 

1.7
---

31

MPW with traumatic amputation of leg, perforations of large and small intestine

Severe 14.5

Surgical amputation, repair

---

---

15,000

Urobil.
Bil.

9.6 3.0

0.5 1.6

8.0 2.0 

21.0 2.7

28.0 3.3

65.0 3.6

7.8 2.7

24.0 2.4

14.5 2.1

18.0 2.4

32

MPW with traumatic amputation of leg

Mod. 9.0

Surgical amputation, repair

100

---

6,000

Urobil.
Bil.

2.9 0.9

7.3 0.4

3.6 
---

2.3
0.4

4.9
---

---
---

---
---

---
---

---
---

---
---

33

MPW, chest, lung

Mod. 3.2

Debridement under local anesthesia

---

---

2,000

Urobil.
Bil.

4.4 1.9

5.8 1.4

3.8 1.4

---
1.0

---
1.0

---
1.3

---
1.2

---
0.7

---
0.8

---
0.8

34

MPW, arms, legs

Mod. 5.7

Debridement

---

---

7,500

Urobil.
Bil.

34.4
4.4

29.8 2.6

37.8 1.6

30.5 1.0

54.0 1.2

23.1 1.7 

36.6 1.1

13.2 0.9 

16.5 0.8

3.3
---

35

MPW, arms, legs

None 4.7

Debridement

---

---

2,500

Urobil.
Bil.

7.3 1.4

5.1 0.8

8.5 0.5

---
0.5

8.6 
0.4

17.1 
---

11.4
---

6.2
---

---
---

---
---

36

MPW, arms, legs

Mod. 4.3

Debridement

---

---

2,000

Urobil.
Bil.

0.9 1.5

2.9 1.1 

1.4 0.8

0.6 
1.1

0.7
1.4

9.5 0.8

5.5 0.9 

---
0.8

---
0.8

---
0.8

37

MPW, abdomen

None 3.3

Negative exploration

---

250

1,500

Urobil.
Bil.

0.8 0.7

---
0.7

0.6 0.5

1.0 
0.8

0.8
0.3 

0.4 0.4

4.3
---

1.4
---

0.5
---

0.3
---

Abbreviations and Symbols
State of Shock and Points--see Appendix
MPW--multiple penetrating wounds

Plasma Bilirubin Concentration is reported as the total concentration
or as the direct over the indirect component in milligrams per 100 milliliters
(normal 0.7 mg. per 100 ml. or less).

Bromsulphalein Retention is reported as the per cent dye retention 45 minutes
after the intravenous injection of 5 mg. of dye per kg. of body weight
(normal 7% retention or less).

Urine Urobilinogen Excretion is reported as the total 24-hour
excretion in milligrams (normal 4.0 mg. or less in 24 hours).


151

(24 casualties), 2.6 mg. after 6 hours (13 casualties), and 2.1 mg. after 12 hours (12 casualties).

Figure 1 demonstrates the changes during resuscitation and for the first 24 hours after surgery.

FIGURE 1.
Average change in the total, direct and indirect plasma bilirubin concentration of 24
battle casualties during and following resuscitation with stored blood.

Of the 24 casualties who had the van den Bergh determination carried out during the first 24 hours after surgery, only 5 showed an elevation of the direct component above 0.3 mg. per 100 ml. of which the highest was 0.8 mg. per 100 ml. At no time did the direct component play a major role in the elevation of plasma bilirubin.

During the first 10 days of convalescence, one of three patterns evolved. In 15 of the 25 casualties studied, a progressive fall occurred, the plasma bilirubin averaging 1.3, 1.0 and 0.8 mg. per 100 ml. on the second, third, and fourth days. Eight of these latter patients demonstrated a continued fall to normal in the plasma bilirubin concentration and thereafter the concentration remained normal during the succeeding week. These eight patients will be referred to as bilirubin group I (Fig. 2). Seven of the fifteen patients who had returned to normal, however, demonstrated a secondary rise between the fourth and eighth day. These seven patients will be referred to as group II (Fig. 2). After this secondary rise, the bilirubin slowly returned toward normal. Finally, seven patients maintained a high bilirubin throughout the 10 days of postoperative observation. These


152

patients will be referred to as group III (Fig. 2). Refer to Tables 5, 6, and 7 for data concerning bilirubin groups.

Bromsulphalein Retention

Bromsulphalein retention was studied in 5 normal unwounded soldiers and in 23 severely injured battle casualties. The retention following injury and resuscitation was frequently marked and persistent.

The retention 45 minutes after the intravenous injection of 5.0 mg. bromsulphalein per kilogram of body weight ranged from 2 per cent to 7 per cent and averaged 5 per cent in the normal controls. The 45-minute retention in the 23 casualties on the first postoperative day ranged from 3 to 42 per cent retention (average 20 per cent) (Table 2). On the third postoperative day, the retention averaged 11 per cent and as a generalization, the subsequent return to normal was gradual for 5 to 10 days thereafter (Table 2).

FIGURE 2.
Daily changes (averages) in total plasma bilirubin
concentration in Bilirubin Groups I, II, and III.

Serial determination revealed a secondary rise in the retention in four patients between the third and sixth days. These were in patients with wounds primarily limited to the abdomen and chest.

Urobilinogen Excretion in Urine

The excretion of urobilinogen in the urine became elevated toward the end of the first week after injury.

Twenty-four-hour excretion of urobilinogen in the urine was studied daily in 13 battle casualties during the first 5 to 14 days following injury. The specimen collected from 0800 hours the first day to 0800 hours the second day was designated as the first day's collection.


153

Control studies were made on the 24-hour urine excretion on 10 laboratory personnel, which demonstrated that the urine urobilinogen excretion of the control subjects never exceeded 4 mg. and was usually less than 2 mg. per 24 hours.

Four of the thirteen casualties demonstrated an early elevation in urobilinogen excretion in the urine (two patients on the second day and two patients on the third day). This rise was moderate in degree (6 to 45 mg. per 24 hours) averaging 22 mg. per 24 hours. This rise was maintained for only 24 hours (Table 3, Fig. 3).

In 11 of the 13 patients, a late rise in urine urobilinogen excretion occurred, the peak elevation being between the fifth and eighth day (averaging 6.5 days). The average excretion on this peak day was 54 mg. in 24 hours with the range between 5 and 224 mg. per 24 hours. This increment in urobilinogen excretion usually persisted for several days before disappearing (Fig. 3).

FIGURE 3.
The typical response of urine urobilinogen and plasma bilirubin following wounding and resuscitation.
Height of peak values and days on which they occurred are averages of all patients.
The early rise in urine urobilinogen excretion occurred in only 4 of 13 patients and
represents only an average of these 4 patients.


154

The urine urobilinogen excretion seemed related to preceding changes in the plasma bilirubin. Twelve of the thirteen patients exhibited an early rise in plasma bilirubin to between 0.9 and 5.5 mg. per 100 ml. (averaging 2.6 mg. per 100 ml.) and 9 of the 13 casualties had a late rise in bilirubin around the fifth day ranging from 0.9 to 5.0 mg. per 100 ml.). Like the urobilinogen excretion, this rise in bilirubin was maintained a few days (average of 2.6 days) before returning to normal (Fig. 3).

Prothrombin Activity

The changes in prothrombin activity as measured by the one-stage test of Quick1 were fairly uniform following wounding and resuscitation. Five casualties at the time of their admission to the forward hospital who had not received blood volume replacement therapy before study was begun demonstrated the normal prothrombin activity. There was, however, a distinct fall in prothrombin activity following transfusion and operation. Twenty-eight casualties were studied and in each there was a "primary fall" in prothrombin activity to an average of 50 per cent of normal activity following resuscitation (variation 37 to 88 per cent). The majority of the casualties (20 of 28) then demonstrated a rise to 90 percent of normal activity or higher between the first and fourth postoperative days (average 2.5 days). The other eight casualties demonstrated a rise but to a lesser degree during this period and reached an average of 61 per cent of normal (variation 37 to 88 per cent) (Fig. 4). In the ensuing days a total of 18 patients were studied for a week or longer (Fig. 4). All had decreased prothrombin activity after the fourth day. Most patients had risen to normal activity and then fallen, others had maintained a persistent defect in prothrombin activity since resuscitation. The average depth of this "secondary fall" was 61 per cent (variation 20 to 87 per cent of normal activity). This decreased activity was most pronounced on the seventh to the eighth postoperative day and by the tenth postoperative day, in most instances, a rise toward normal activity had begun. Some casualties had reached normal activity by the tenth day.

Cephalin Flocculation

The degree of cephalin flocculation (24-hour test of Hanger21) was studied in 15 normal soldiers and 22 battle casualties.

Twelve casualties were studied prior to therapy (Table 4). All six casualties who were not in shock demonstrated a normal flocculation (one plus flocculation or less in 24 hours), whereas four of the six


155

FIGURE 4.
Prothrombin activity in per cent of normal activity following wounding resuscitation.
The maximum, minimum and average daily values of 18 battle casualties.
Note the "primary fall" in prothrombin activity immediately after surgery with subsequent
rise to normal between the first and fourth day. This rise to normal is followed
by a "secondary fall" as shown by the average curve.

who were in shock demonstrated a strongly positive reaction (three or four plus) prior to therapy.

Following the onset of resuscitation with whole blood, the cephalin flocculation increased rapidly. Bank blood itself demonstrated a flocculation of two plus to four plus in 24 hours (determinations on eight bottles taken at random). It should be noted, however, that the flocculation became abnormal in the critically injured casualty prior to transfusion.

Seventeen of twenty casualties studied within 12 hours after operation had an abnormal reaction (Table 4).

Twenty-one casualties were studied during the period of convalescence. Characteristically, they demonstrated a two plus reaction immediately after operation which increased to three plus or four plus after 24 to 48 hours. The reaction then characteristically slowly returned to normal during the ensuing week. The average time required for the reaction to revert to normal was 6 days. However, two casualties still demonstrated a positive test when evacuated on the ninth and eleventh days respectively. Once the reaction returned to normal, it tended to remain there, but 8 of the 21 patients had a transient secondary increase in flocculation of approximately 1 day's duration. This secondary rise usually followed secondary transfusion.


Table 4.

Patient Number

Injury

Shock Points

Operation

Total ml. Therapy

Albumin

Plasma

Blood

1

MPW, legs, small intestine, bladder

Mod. 
5.4

Debridement, repair

100

---

1,000

3

MPW, small intestine, legs, laceration of vena cava.

Severe 12.5

Debridement, repair

200

---

10,500

4

MPW, chest, diaphragm, liver

None
8.4

Debridement, repair

---

---

---

5

MPW, small intestine, large retroperitoneal hematoma

None
4.3

Repair

100

---

1,500

6

Perforation of stomach

None
4.2

Repair

---

500

2,000

7

Perforation of diaphragm, liver

None
6.8

Repair

---

---

1,500

8

MPW with fracture of tibia and radius.

None
2.7

Debridement

---

500

1,000

9

MPW, colon, kidney

None
5.3

Nephrectomy, repair of colon.

100

---

1,500

19

Traumatic amputation above knee.

Severe
6.5

Surgical amputation

100

---

4,000

20

Traumatic amputation above knee.

Mod. 
6.0

Surgical amputation

---

---

6,500

23

Bilateral traumatic amputation below knees.

None
5.7

Surgical amputation

200

500

6,500

24

MPW, small intestine, ureter

Mod. 
8.0

Repair, anastomosis of ureter.

100

---

2,500

25

Traumatic amputation of foot

None
3.7

Surgical amputation

---

---

1,000

26

Bilateral traumatic amputation below knee.

Mod. 
10.6

Surgical amputation

---

---

9,500

27

Laceration of iliac artery, colon

Mod. 
5.1

Repair

100

500

6,000

28

MPW, liver, stomach, colon, diaphragm.

Severe 10.2

Repair

100

---

5,500

29

MPW, legs, traumatic amputation of foot.

Severe 
8.5

Debridement, surgical amputation.

200

---

7,000

33

MPW, chest, lung

Mod.
3.2

Debridement under local anesthesia.

---

---

2,000

34

MPW, arms, legs

Mod. 
5.7

Debridement

---

---

7,500

35

MPW, arms, legs

None 
4.7

Debridement

---

---

2,500

36

MPW, arms, legs

Mod. 
4.3

Debridement

---

---

2,000

37

MPW, abdomen

None
3.3

Negative exploration

---

250

1,500

Abbreviations and Symbols
State of Shock and Points-see Appendix
MPW-multiple penetrating wounds


Cephalin Flocculation
 

Hours Postoperative

Days Postoperative

0

6

12

24

2

3

4

5

6

7

8

9

10

---

---

3.4

---

3.4

1.1

±.1

2.2

1.1

1.1

---

---

---

2.2

2.2

---

---

4.4

4.4

4.4

---

3.4

3.4

3.4

3.4

3.4

---

---

---

3.3

4.4

3.4

4.4

---

3.4

3.3

3.3

2.3

---

---

---

3.3

---

3.4

2.3

---

2.3

2.3

1.1

2.3

---

---

---

---

3.3

---

3.3

3.3

---

2.2

2.3

1.2

1.2

---

---

3.3

---

---

3.4

4.4

2.2

2.2

2.2

1.1

3.3

---

---

---

2.2

---

3.3

---

3.3

---

3.3

1.3

1.1

1.2

---

---

---

---

---

3.4

---

4.4

3.4

4.4

---

---

---

---

---

---

2.2

---

3.3

---

3.3

---

3.4

---

1.3

1.2

---

---

---

---

---

3.3

---

3.3

2.2

2.3

---

2.2

1.2

---

---

---

3.3

---

---

3.3

3.4

3.3

3.2

1.2

1.1

3.3

1.2

---

---

---

---

2.3

---

3.3

2.3

2.2

2.2

1.2

1.2

2.2

---

---

2.3

---

---

3.3

2.3

1.2

3.3

1.2

1.1

1.2

0

0

---

---

---

4.4

---

0. ±

±.2

---

---

1.1

±.1

±.1

±.1

---

---

---

0. ±

---

3.3

---

3.3

3.3

3.3

1.1

±.1

1.1

0

---

---

3.3

---

---

3.4

2.3

1.1

1.1

±.1

1.2

0

---

---

---

---

3.4

3.3

3.3

1.2

2.3

±.1

---

---

---

---

3.4

3.3

2.3

2.3

3.3

---

2.3

2.2

---

---

2.2

1.2

±.1

1.3

2.3

±.1

2.2

---

±.2

---

---

2.2

±.1

±.1

---

---

2.3

1.2

2.2

1.2

±.1

---

---

±.2

---

---

1.2

2.2

2.3

3.3

3.3

2.2

1.2

1.2

---

1.1

---

1.2

1.1

1.1

±.1

±.1

±.1

---

2.3

2.3

±.1

1.2

±.1

---

±.1

2.3

---

±.1

±.1

The Cephalin Flocculation Reaction is reported as the 24-hour and 48-hour reaction. Top normal flocculation is considered to be one plus in 48 hours.


156

Correlation of the data revealed that only patients with peripheral wounds suffering shock or abdominal wounds with or without shock maintained an abnormal cephalin flocculation reaction past the fifth day. Patients with peripheral wounds not suffering shock did not maintain an abnormal reaction past the fifth day.

There did not appear to be a significant positive correlation between the duration of an abnormal reaction and the amount of blood a casualty had received or the total amount of trauma as we estimated it.

Thymol Turbidity

Twelve moderately and severely wounded casualties (Table 1, Patients 26 through 37) were studied daily for 7 to 10 days following injury. At no time did any of the patients show an abnormal elevation in the thymol turbidity reaction. Daily normal determinations on a total of 10 healthy hospital personnel never exceeded four units.

Discussion

As previously stated, it would be ideal to interpret hepatic function on the basis of the vital functions of the liver, such as the production of energy, metabolism of pigment, protein, carbohydrate, fat, toxins, citrate, morphine, pentothal, hormones, urea and other substances such as cholinesterase and the vasodepressor material of Shorr.

The questions we would like to answer are: Is the liver working effectively? Do alterations in hepatic function as measured by our present-day tests represent actual insufficiency or a deviation of functions to those more vital to the injured patient? This paper will not answer all of these questions. It is hoped, however, that it can document the alterations observed and be of help as a guide to further study in determining the role of the liver in response to injury.

It is obvious from our studies on these cases that a combination of factors are operating that could influence hepatic function itself or alter the results and interpretation of the hepatic function tests as we know them. To mention but a few of the variables-the original tissue injury, secondary anoxic injury, the administration of plasma, saline, albumin or stored blood, the trauma of anesthesia and operation and the effects of continued antibiotic therapy, as well as electrolytic and hormonal changes.

This great interplay of factors makes definitive interpretation difficult or impossible, but an effort will be made to point out the implications of the pattern of response observed.


157

The metabolism of bile can be considered to be a vital function of the liver. In the severely injured casualty, two factors of prime importance in interpreting the change observed are to appreciate the load of pigment metabolism placed on the liver through massive transfusion and extensive muscle damage and to attempt to evaluate the ability of the liver to handle this increased load.

Bilirubin (Tables 5-9)

The effect of injury per se on plasma bilirubin cannot be detected from these studies. Only one of the casualties studied was admitted as late as 9 hours after injury and this was the only casualty with an elevated plasma bilirubin prior to transfusion. Beecher et al,25 described a progressive, low-grade rise in plasma bilirubin of the battle casualty prior to transfusion. These authors worked during an evacuation time of 1 to 24 hours and attributed the rise in plasma bilirubin to the probable absorption and metabolism of extravasated, hemolyzed blood.

Following whole blood replacement, there is a marked, immediate rise in the plasma bilirubin (Fig. 1). This increment is predominantly in the indirect, protein-bound fraction. This would suggest that at least part of the elevation in the plasma bilirubin concentration was due to increased metabolism of hemolyzed blood. More recent work, however, suggests that the direct reacting "l minute" bilirubin fraction is not a chemically distinct entity which can be differentiated from indirect bilirubin by its physiochemical properties.6 These workers suggest that the "1 minute" bilirubin level is an arbitrarily selected point on the ascending limb of a diphasic curve representing the rate of azo-bilirubin development in the direct van den Bergh reaction. They feel that the rate of diazotization is determined by the concentration of bilirubin and by physical or chemical factors in blood.


158

Table 5. Bilirubin Group I

(Patients who had a return of bilirubin to normal by the fourth day and remained normal)

Patient Number

Injury

Shock Points

Total ml. Blood

BSP

Lowest* Prothrombin

Day 
C. F.** Normal

First Postop. Day

Third Postop. Day

4

MPW, chest, diaphragm, liver

None
8.4

2,000

19

14

80

9+

5

MPW, small intestine, large retroperitoneal hematoma

None
5.3

1,500

16

10

70

8+

6

Perforation of stomach

None
4.2

2,000

12

5

75

8

7

Perforation, diaphragm, liver

None
6.8

1,500

5

4

95

6

8

MPW with fracture of tibia and radius

None
2.7

1,000

---

4

80

5

15

MPW, shoulder

None
5.7

3,000

---

---

---

---

23

Bilateral traumatic amputation below knees

None
5.7

6,500

---

---

4.3

5

25

Traumatic amputation of foot

None
3.7

1,000

---

---

55

5

29

MPW, legs, trauma-amputation of foot

Severe 
8.5

7,000

18

9

60

6

30

Quadruple traumatic amputations

Mod.
11.9

11,000

4

6

---

---

35

MPW, arms, legs

None
4.7

2,500

---

---

---

1

 

 
Average
 


5.2

 


3,500

 


12

 


7

 


62

 


6

*Average low prothombin activity in per cent of normal after the fourth day.
**Day on which the cephalin flocculation reached normal (1+ or less).
Abbreviations and Symbols
State of Shock and Points-see Appendix.
MPW-multiple penetrating wounds.
Plasma Bilirubin Concentration is reported as the total concentration or as the direct over the indirect component in milligrams per 100 milliliters (normal 0.7 mg. per 100 ml. or less).
Bromsulphalein Retention is reported as the per cent dye retention 45 minutes after the intravenous injection of 5 mg. of dye per kg. of body weight (normal 7 per cent retention or less).


159

Table 6. Bilirubin Group II

(Patients whose plasma bilirubin had returned to normal by the fourth day but rose to abnormal levels after the fourth day)

Patient Number

 


Injury

Shock Points

Total ml. Blood

Day of Peak Value

Peak Value

Days Duration of Elevation

BSP

Lowest* Prothrombin

Day C.F.** Normal

First Postop. Day

Third Postop. Day

1

MPW,* legs, small intestine, bladder

5.4

1,000

5

.5/.7

3+

---

---

60

4

3

MPW, small intestine, legs, laceration of vena cava

Severe
12.5

10,500

7

.2/1.2

5

27

11

57

11+

9

MPW, colon, kidney

None
5.3

1,500

7

.2/.7

1+

21

17

58

5+

11

MPW, fracture both femurs

Mod.
12.0

9,500

9

1.1/1.9

5+

19

11

---

8+

24

MPW, small intestine, ureter

Mod.
8.0

2,500

6

.5/.5

1

---

---

30

6

26

Bilateral traumatic amputations below knees

Mod.
10.6

9,500

4

0/.9

1

5

1

16

2

36

MPW, arms, legs

Mod.
4.3

2,000

5

.1/1.3

6

---

---

---

1

37

MPW, abdomen

None
3.3

1,500

4

.1/.8

1

12

---

---

2

 

     
    Average

 


7.6

 


4,200

 


6

 


1.3

 


3.6

 


17

 


10

 


56

 


6

*Average low prothrombin activity in percent of normal after the fourth day.
**Day on which the cephalin flocculation reaction reached normal (1+ or less).
Abbreviations and Symbols
State of Shock and Points-see Appendix
MPW-multiple penetrating wounds
Plasma Bilirubin Concentration is reported as the total concentration or as the direct over the indirect component in milligrams per 100 millimeters (normal 0.7 mg. per 100 ml. or less).
Bromsulphalein Retention is reported as the per cent dye retention 45 minutes after the intravenous injection of 5 mg. of dye per kg. of body weight (normal 7 percent retention of less).


160

Table 7. Bilirubin Group III

Patients who continued to have an abnormal plasma bilirubin past the fourth day
 

Patient Number

Injury

Shock Points

Total ml. Blood

Day of Peak Value

Peak Value

Days Duration of Elevation

BSP

Lowest* Prothrombin

Day C.F.** Normal

First Postop. Day

Third Postop. Day

21

Laceration, liver

Mod.
7.8

4,000

8

6.6

10+

25

8

43

---

27

Laceration of iliac artery, colon

Mod.
5.1

6,000

6

2.0/2.9

10+

27

31

20

7

28

MPW, liver, stomach, colon, diaphragm

Severe
10.2

5,500

5

.2/1.4

7

21

22

43

5

31

MPW with traumatic amputation of leg, perforations of large and small intestine

Severe
14.5

15,000

7

.4/2.9

10+

40

14

50

---

33

MPW, chest, lung

Mod.
3.2

2,000

6

.1/1.2

8

---

---

---

9

34

MPW, arms, legs

Mod.
5.7

7,500

6

.4/1.3

9+

---

---

---

3

 

 
Average
 


7.7

 


6,600

 


6.4

 


3.3

 


10

 


28

 


18

 


39

 


6

*Average low prothrombin activity in per cent of normal after the fourth day.
**Day on which the flocculation reaction reached normal. (1± or less).
Abbreviations and symbols
State of Shock and Points-see Appendix
MPW-multiple penetrating wounds
Plasma Bilirubin Concentration is reported as the total concentration or as the direct over the indirect component in milligrams per 100 milliliters (normal 0.7 mg. per 100 ml. or less).
Bromsulphalein Retention is reported as the per cent dye retention 45 minutes after the intravenous injection of 5 mg. of dye per kg. of body weight (normal 7 per cent retention or less).


161

The plasma hemoglobin of stored blood studied on 300 pints of bank blood used on these casualties revealed an average of 34 mg. of hemoglobin per 100 ml. of plasma.7 Eleven patients were studied on admission and all were found to have a normal plasma hemoglobin except for one patient who was receiving whole blood transfusion at the time of admission.

Twenty-two patients were studied after transfusion and operation. These casualties (most of whom are included in this study) had received between 2 and 37 pints of blood. The plasma hemoglobin concentration of these patients averaged 18 mg. per 100 ml. and ranged between 1.2 and 102 mg. per 100 ml. immediately after operation.23 The elevation in plasma hemoglobin characteristically disappeared during the ensuing 12 hours after operation.

It was observed from this study that, whereas the peak in plasma hemoglobin occurs during or immediately after transfusion, the peak in plasma bilirubin occurs several hours later.

In untraumatized individuals, it has been shown9 that the injection of free hemoglobin sufficient to produce a plasma hemoglobin value of 60 to 130 mg. per 100 ml. also produces an elevation in total bilirubin above control values of only 0.2 mg. per 100 ml. When the plasma hemoglobin was raised to 150 mg. per 100 ml., the bilirubin might reach 1.2 mg. per 100 ml. None of the patients in our study demonstrated a plasma hemoglobin as high as 150 mg. per 100 ml., but almost all demonstrated a bilirubin value well above 1.2 mg. per 100 ml.

Other work27 demonstrated that the initial rise in bilirubin occurs within 30 minutes after the injection of hemoglobin, reaches its maximum within 2 to 3 hours and returns to normal within 5 to 8 hours. Again the pattern of response was different in the severely injured soldier and was characterized by a longer period of abnormality. It can be theorized that the load of plasma hemoglobin imposed on the patient was greater, but our data on plasma hemoglobin did not substantiate this. It could also be theorized that there was some degree of liver impairment which delayed the metabolism of the bile pigments. The latter is a likely possibility. Although the plasma hemoglobin concentration was not very high, much blood was lost into the tissues. Its subsequent metabolism may have accounted, in part, for the sustained increase in plasma bilirubin.

Scattergraphs failed to show a positive correlation between initial elevation, late elevation or the planograph area of abnormality of the plasma bilirubin and the magnitude of transfusion. Both the impairment of hepatic function (as influenced by the degree and duration of shock) and the load of pigment imposed on the circulation (magnitude of transfusion) must certainly be factors which are inseparable with the methods and data available.


162

In analyzing the response of the three arbitrary groups there appeared other positive correlations (Table 8). Group I was characterized by having a high incidence of peripheral wounds (65 per cent), a low incidence of shock (20 per cent), a small transfusion volume (3,500 ml.), a small bromsulphalein retention on the first and third days (12 and 7 per cent) and a small "secondary fall" in prothrombin activity (to 62 per cent of normal). Group III was characterized by having a high incidence of abdominal wounds (67 per cent), a high incidence of shock (100 per cent), a large transfusion volume (6,500 ml.), a large bromsulphalein retention on the first and third days (28 and 18 percent) and a marked "secondary fall" in prothrombin activity (to 39 per cent of normal). Group II fell in the middle of all categories.

Table 8. Correlation of Data on Bilirubin-Groups I, II, and III
 

 


Variables

Group

I

II

III

Number of patients in each group

11

8

6

Per cent of group with abdominal wounds

35

62

67

Per cent of group with peripheral wounds

65

38

33

Per cent of group suffering shock

20

60

100

Average number ml. blood received

3,500

4,500

6,500

BSP retention first day-per cent

12

17

28

BSP retention third day-per cent

7

10

18

Average prothrombin activity during secondary fall (% of normal activity)

62

56

37

Day on which cephalin flocculation returned to normal (average)

6

6

6

Again the variables would be difficult to separate, but it does appear that shock and abdominal wounds predispose to a more marked deviation in the hepatic function tests. The rapid clearance of bilirubin in the untraumatized individual27 would suggest that some degree of liver impairment was operating in the traumatized soldiers to account for the sustained elevation in plasma bilirubin concentration.

Other investigators22 have demonstrated an elevated bilirubin in 24 of 33 patients undergoing elective surgery. In their experience there was no correlation between duration or degree of abnormal plasma concentrations of bilirubin and the occurrence of shock during operation. They did suggest a correlation between the elevation and the amount of blood given.


163

Bromsulphalein Retention

Bromsulphalein retention, prior to transfusion therapy, was not studied in this series. Beecher et al.,25 however, demonstrated a mild retention (average 8 per cent) in 15 patients studied prior to plasma therapy and a slightly higher retention (average 14 per cent) in 25 patients requiring plasma but studied before whole blood transfusion. They demonstrated a lower retention the day following whole blood transfusion than was noted prior to therapy.

The retention of dye in the patients of this series was as high as 42 per cent on the first post operative day (Table 2). Although this retention may have been in part on the basis of competition for storage and excretion with the plasma hemoglobin-bilirubin compounds, impairment of hepatic function appears evident.

On the first or second postoperative day, the bromsulphalein retention was usually accompanied by an elevated plasma bilirubin. Some investigators believe that bilirubin and bromsulphalein compete for excretion and that in the presence of an elevated bilirubin there will always be abnormal bromsulphalein retention.11 Other investigators disagree with this contention and believe that the two compounds do not compete for excretion to the extent that an elevation in bilirubin will cause abnormal bromsulphalein retention.24 Geller observed in a group of 22 postoperative patients that there occurred an abnormal bromsulphalein retention in 17 and that 5 of the latter did not have concomitant elevation in bilirubin.22

Twenty-two simultaneous comparisons of bromsulphalein retention and plasma bilirubin concentration were made after the second post-operative day on 14 patients (Table 9).

In eight instances (36 per cent) there was an abnormal retention of bromsulphalein after the bilirubin concentration had returned to normal. These observations indicate that at least some of the retention of bromsulphalein occurs independently of elevation in the plasma bilirubin and is, therefore, probably not on the basis of simple competition for excretion.

Aside from the problem of the elevation in bilirubin, the normal clearance of bromsulphalein is thought to be dependent upon a competent reticuloendothelial system.8, 9, 26

Klein8 found abnormal bromsulphalein retention after splenectomy but not after laparotomy. Mills9 confirmed these studies and showed that India ink, when injected intravenously, jammed the Kupffer system and was accompanied by an increased bromsulphalein retention.


164-165

Table 9. Correlation of Simultaneous Determinations of BSP and Plasma Bilirubin
 

Patient Number

Injury

Shock and Points

Total ml. blood

Day Postop. of first Comparison

BSP Retention

Plasma Bilirubin

Day Postop. of second Comparison

BSP Retention

Plasma Bilirubin

3

MPW, small intestine, legs, laceration of vena cava

Severe
12.5

10,500

3

11

0.7

6

21

0.9

4

MPW, chest, diaphragm, liver

None
8.4

---

3

14

0.7

6

24

0.4

5

MPW, small intestine, large retroperitoneal hematoma

None
4.3

1,500

3

10

.1/.7

8

8

.1/.4

6

Perforation of stomach

None
4.2

2,000

3

5

.1/.7

8

5

.1/.6

7

Perforation, diaphragm, liver

None
6.8

1,500

3

4

0/.2

6

6

.1/.1

8

MPW with fracture of tibia and radius

None
2.7

1,000

3

4

.1/.3

---

---

---

9

MPW, colon, kidney

None
5.3

1,500

3

17

.2/.1

4

6

Norm.*

11

MPW, Fracture both femurs

Mod.
12.0

9,500

3

11

.2/1.1

---

---

---

21

Laceration of liver

Mod.
7.8

4,000

3

8

1.2

---

---

---

26

Bilateral traumatic amputation below knee

Mod.
10.6

9,500

3

1

0/.8

6

1

0/.5

28

MPW, liver, stomach, colon, diaphragm

Severe
10.2

5,500

3

28

.1/1.7

8

21

Norm.*

29

MPW, legs, traumatic amputation of foot

Severe
8.5

7,000

4

9

0/.6

---

---

---

30

Quadruple traumatic amputations

Mod.
11.9

11,000

3

6

0/.5

---

---

---

31

MPW with traumatic amputation of leg, perforations of large and small intestine

Severe
14.5

15,000

3

14

.1/1.9

---

---

---

*Bilirubin not determined on that day but preceding or subsequent volumes normal.
Abbreviations and Symbols
State of Shock and Points-see Appendix
MPW-multiple penetrating wounds
Plasma Bilirubin Concentration is reported as the total concentration or as the direct over the indirect component in milligrams per 100 milliliters (normal 0.7 mg. for 100 ml. or less).
Bromsulphalein Retention is reported as the per cent dye retention 45 minutes after the intravenous injection of 5 mg. of dye per kg. of body weight (normal 7% retention or less).


166

The large amount of free hemoglobin received during transfusion may well "jam" the Kupffer system and prevent the removal of bromsulphalein from the blood before its excretion by the liver. The normal bilirubin values in the eight patients with residual bromsulphalein retention make it unlikely that the reticuloendothelial system is still filled with hemoglobin.

Only those patients with abdominal wounds or those with extremity wounds complicated by severe shock demonstrated a retention over 20 per cent on the first postoperative day. The patients with abdominal wounds tended to demonstrate a greater retention than did the patients with extremity wounds. Thus on the first postoperative day, there is a distinct relationship between the degree of shock, type of wound and average bromsulphalein retention (Table 10).

Table 10. Average Bromsulphalein Retention on the First Day Post-injury
 

 

Degree of shock

Location of Wounds

Abdominal Injury

Extremity Injury

Number Points

Per cent BSP Retention

Number Points

Per cent BSP Retention

Severe

3

30

4

22

Moderate

3

27

5

9

None

6

14

1

4

Regardless of the location of the wounds, there seemed to be an exaggeration of the bromsulphalein retention in the patients who had been in shock and who had received the largest quantities of blood.

The duration of the impairment in hepatic function is indicated by the marked retention of dye (15 to 22 per cent) in four patients when last studied on the ninth and eleventh day after injury.

Finally, there appears to be a positive correlation between the secondary depression of prothrombin activity and the bromsulphalein retention during the first week after injury (Fig. 5). These two abnormalities coupled with an elevation in urine urobilinogen excretion may well represent hepatic dysfuntion.


167

FIGURE 5.
A correlation between the degree of bromsulphalein retention on the
third postoperative day and the depth of fall in prothrombin activity during
the late depression in prothrombin activity.

Urine Urobilinogen

It has been observed that the administration of antibiotics will produce a marked elevation in stool bilirubin and complete elimination of urobilinogen from the stool.13 Antibiotic therapy, as used on these casualties, might, therefore, tend to lower the urinary urobilinogen. The high values observed thus take on added significance. Although quantitative comparisons are of doubtful value, patterns of change become evident. For example, 4 of 14 patients had an early rise and 11 of 13 patients had a late rise in urine urobilinogen excretion (Fig. 3). Either rise could have been on the basis of increased pigment metabolism following breakdown of hemoglobin or on the basis of transient hepatic dysfunction. It is worthy of note that the late spike in urine urobilinogen usually correlated with the secondary peak in plasma bilirubin and with the depth of depression of prothrombin activity. This triad of abnormality may represent hepatic insufficiency which reaches its peak about a week after injury.


168

Prothrombin

The typical response of a "primary fall" in prothrombin activity following resuscitation, followed by a spontaneous rise to normal or near normal activity and then a "secondary fall" was described earlier in this paper and has been described elsewhere in detail.2 In an attempt to define the changes in prothrombin activity, various analyses were carried out.

The daily administration of 100 mg. of vitamin K intramuscularly or intravenously did not produce any change in this pattern of depressed activity. Intensive studies in 11 casualties2 revealed that the platelet count, plasma fibrinogen, and clotting time in silicone showed no alteration that could account for or correlate with the depression of prothrombin activity. The platelet count was either normal or slightly elevated in the immediate postoperative period and rose gradually to reach its maximum value, which was two to three times normal, on about the fifth or sixth day before it fell toward normal on about the tenth day. The plasma fibrinogen was usually normal or slightly elevated in the immediate postoperative period, and it rose markedly to levels two to three times normal (Fig. 6). The shortening of the clotting time,3, 15, 28, 29 rise in platelets4 and rise of plasma
fibrinogen5, 17 following stress have been observed previously.

During the "primary fall" in prothrombin activity, it was observed that the patient's plasma was unable to correct the labile factor (accelerator-globulin) deficiency of stored plasma.2 It was also observed that the addition of deprothrombinized plasma, containing adequate

FIGURE 6.
Plasma fibrinogen concentration following wounding and resuscitation with stored blood.
An average of 10 moderately or severely wounded battle casualties. The only subnormal
value occurred immediately after operation but corrected itself within 12 hours after surgery.


169

labile factor, increased the prothrombin activity of the patient's plasma (in vitro). These observations indicate that during the first 2 to 4 days postoperatively, the "primary fall" in prothrombin activity is probably on the basis of the labile factor deficiency. Stored bank blood itself is deficient in labile factor.16 By the time of the "secondary fall," the labile factor deficiency had been corrected spontaneously. The mechanism for the late depression in prothrombin activity was not definitely established but a qualitative defect in the platelet was suspected.2 A deficiency of prothrombin per se was ruled out in some patients but not in others. At least a pure prothrombin deficiency, in contradistinction to a defect in the over-all prothrombin mechanism, could not be proved as the cause of the secondary fall in prothrombin activity.

Cephalin Flocculation

As described earlier, the cephalin flocculation reaction was abnormal (greater than one plus in 24 hours) in four of six casualties admitted to the hospital in shock. Theoretically, an abnormal cephalin flocculation reaction denotes an abnormal quantitative relationship between the albumin and globulin fractions.18 The occurrence of an abnormal cephalin flocculation on admission probably does not represent hepatic damage at this early time. Rappaport19 has demonstrated that acute hepatic coma in dogs, resulting in death, is not accompanied by abnormal electrophoretic patterns of plasma. At least in the dog, injury resulting in acute hepatic failure would not allow time for an abnormal cephalin flocculation reaction to develop. Theoretically, either the loss of albumin by metabolism or extravasation or an increase in globulin through mobilization or synthesis could account for this early abnormal reaction. Further study by members of the Research Team demonstrated an early, consistent drop in plasma albumin concentration.34 The observed drop in plasma albumin concentration may well be the cause of this increased flocculation.

As to the continuing abnormality in flocculation during the first week, two mechanisms could be in operation, either vascular shifts of protein or hepatic insufficiency. Rappaport19 and Chanutin20 have shown that hepatic ischemia or partial hepatectomy in dogs and rats results in changes in the electrophoretic pattern, indicative of low albumin and an abnormally high globulin and fibrinogen from the third to the thirtieth postoperative day. Following simple laparotomy, the abnormal picture was corrected by the eighteenth postoperative day. It was observed by members of the Research Team that following wounding, the plasma fibrinogen increases to about twice normal and remains elevated 10 days or longer.2 The elevation


170

in plasma fibrinogen has been considered by some to represent a normal response to injury.5 A rise in the total globulin following injury has also been reported20 and may also be a normal response to injury. The changes in the globulin concentration in the plasma of the Korean casualties were found to be variable but the fall in albumin concentration was predictable.34

The continuation of the abnormal cephalin flocculation may thus be on the basis of the normal elevation of plasma globulin concentration following injury and may be evidence of a normal response to injury. Conversely, the abnormal cephalin flocculation reaction in the battle casualty may not be on the basis of an elevation in globulin but may represent a continued depression in albumin following injury. The duration of an abnormal cephalin flocculation reaction does not correspond with the duration of abnormality of other hepatic function tests in the battle casualty. The cephalin flocculation reaction returned to normal, as an average, on the same day in the patients of bilirubin Groups I, II, and III (Table 8). The duration of abnormal cephalin flocculation reaction appeared, therefore, to be independent of changes in bilirubin concentration, prothrombin activity or bromsulphalein retention. There was a suggestion of a correlation between the severity of trauma and the length of time the cephalin flocculation was abnormal. The more severe the trauma, the more marked seemed the response and the longer the cephalin flocculation reaction remained abnormal. Tagnon12 reported that 5 of 20 patients undergoing elective surgery developed abnormal cephalin flocculation reactions postoperatively.

The changes in protein concentrations and the positive flocculation test may therefore represent changes in the wound and circulation rather than deficiencies in hepatic function. The test of hepatic function might more logically consist of the duration required for the liver to reverse the altered protein pattern.

The data on hand do not permit a definitive conclusion as to the mechanism involved in the early preoperative or in the late prolonged abnormality in cephalin flocculation. It cannot be related entirely to the infusion of banked blood.

Thymol Turbidity

The normality of the thymol turbidity in 10 moderately or severely wounded patients during the first 10 days after injury is difficult to interpret. According to Lawler,18 an abnormal thymol turbidity is dependent on an abnormally high globulin fraction. If this is true, it would indicate that our patients did not have an abnormally high globulin and so the abnormal cephalin flocculation reaction probably


171

resulted from a low albumin fraction. Tagnon,12 in reporting on 20 patients undergoing elective surgery (see preceding section), stated that none developed thymol turbidity reactions. Definitive interpretation must be postponed pending further study.

Other Studies

As has been previously pointed out, following injury there is a depletion of the glycogen content of the liver.30 This is associated with an elevated blood glucose level and presumably represents the effort of the organism to mobilize glycogen for energy production. Studies done by the Surgical Research Team confirmed the observation of a diabetic-type glucose tolerance curve for several days after injury.31 Furthermore, they demonstrated the resistance of the diabetic-type glucose tolerance curve to insulin following trauma.31 Normally, there is a 50 per cent drop in fasting blood sugar when 0.1 unit of insulin per kilogram of body weight is given intravenously. For several days after severe injury this drop was found to be only 28 to 30 per cent instead of the normal 50 per cent decrease. This presumably is a normal response of the liver, since it is normal to mobilize glucose rather than to store glycogen during times of stress.

Studies by Snyder32 have correlated the decrease in plasma cholinesterase with the clinical degree of hepatic injury. Following severe trauma, the battle casualty demonstrated only slight diminution of concentration of plasma cholinesterase.33

Serial assays of circulating ferritin (VDM and VEM) have been carried out on several of the casualties studied and will be reported later.

Summary

There was, as a generalization, a typical pattern of response for each of the various hepatic functions studied.

The plasma bilirubin was normal in the unresuscitated casualty for the first 3 to 5 hours after injury. With delay in resuscitation for as much as 9 hours or with the onset of blood transfusion, the plasma bilirubin concentration became elevated. This elevation was in the indirect protein-bound component. Following resuscitation, a variable pattern evolved. In some patients, the plasma bilirubin concentration returned to normal and remained normal; in others the concentration returned to normal but again rose; and in still others the concentration remained elevated throughout the period of observation. The pattern of bilirubin response was more closely correlated with the occurrence of shock and the location of wound than with the


172

amount of blood a casualty had received or the magnitude of tissue injury. Variations in the load of pigments placed on the liver and in the degree of hepatic damage undoubtedly play a part in the observed elevations in bilirubin.

The bromsulphalein retention was usually elevated on the first postoperative day. As a rule, the most marked retention was in the battle casualty who had suffered shock or who had received an abdominal wound. On succeeding days, the bromsulphalein retention usually returned to normal by the third to sixth postoperative day. Some casualties, however, continued to demonstrate an abnormal retention throughout the period of observation.

A small portion of the casualties demonstrated an elevation in urine urobilinogen on the first or second day after injury. The majority of the casualties demonstrated a pronounced rise on the sixth or seventh day after injury.

The plasma prothrombin activity was depressed to approximately 50 per cent of normal following wounding and resuscitation with stored blood. This depression was usually followed by a rise to normal by the third or fourth day. After the fourth day prothrombin activity again became depressed. This second depression prothrombin activity was most marked about the seventh day and usually returned to normal by the tenth day. Vitamin K in massive doses did not affect this pattern of response.

The primary fall in prothrombin activity is probably on the basis of a labile factor deficiency induced by the administration of stored blood, itself deficient in labile factor. The mechanism of the secondary fall in prothrombin activity was not proven but a qualitative deficiency within the platelet was suspected.

Prior to the onset of resuscitation, the casualty in shock characteristically had an abnormal cephalin flocculation reaction. Following transfusion and operation, there was a consistent elevation in the abnormal cephalin flocculation reaction for several days. The mechanism of the elevation may be on the basis of an elevated globulin or a low plasma albumin concentration. These changes in the protein fractions could represent a "physiologic response to injury" or could represent the inability of the liver to replace the albumin stores lost or metabolized at the time of injury.

Thymol turbidity remained normal throughout the phase of recovery.

The synthesis of fibrinogen, glucose and cholinesterase, as studied in conjunction with this work, appears essentially normal.


173

Conclusion

Severe trauma places upon the liver an added burden of tremendous magnitude. The inadequacies of our resuscitative agents add to this burden.

The liver, like every other organ in the body, responds to severe trauma. In general, it appears to respond well to the task of supplying energy for the body and building blocks for the wound. It is not surprising that, with such a wide span of function, certain abnormalities in standard function tests are found. These abnormalities may represent a transient deficiency in hepatic function or may be the result of a deviation of hepatic function into more vital channels.

References

1. Quick, A. J.: The Physiology and Pathology of Hemostasis. Lea & Febiger, Philadelphia, 1951.

2. Scott, R., Jr., and Crosby, W. H.: The Changes in the Coagulation Mechanism Following Wounding and Resuscitation with Stored Blood. To be published.

3. Cannon, W. B., and Gray, H.: Factors Affecting the Coagulation Time of Blood. Am. J. Physiol. 34: 323, 1914.

4. Warren, R., Amdur, M. O., Delko, J., and Baker, D. V.: Postoperative Alterations in the Coagulation Mechanism of the Blood. Arch. Surg. 61: 419, 1950.

5. Ham, T. H., and Curtis, F. C.: Plasma Fibrinogen Response in Man, the Influence of Nutritional State Induced Hyperpyrexia, Infectious Disease, and Liver Damage. Medicine 17: 413, 1938.

6. Klatskin, G., and Drill, V. A.: The Significance of the "One Minute" (Prompt Direct Reacting) Bilirubin in Serum. J. Clin. Invest. 29: 660, 1950.

7. Crosby, W. H.: Report to the United States Army on Survey of Bank Blood in Korea, 1953.

8. Klein, R. I., and Levinson, S. A.: The Removal of Bromsulphalein from the Blood Stream by Reticulo-endothelial System, Proc. Soc. Exper. Biol. & Med. 31: 179, 1933.

9. Mills, M. A., and Dragstedt, C. A.: Bromsulphalein Dye Retention Test as a Measure of Functional Activity of the Reticulo-endothelial System. Proc. Soc. Exper. Biol. & Med. 34: 228, 1936.

10. Cohn, C., Levine, R., and Streicher, D.: The Rate of Removal of Intravenously Injected Bromsulphalein from the Liver and Extrahepatic Tissue of the Dog. Am. J. Physiol. 150: 299, 1947.

11. Dragstedt, C. A., and Mills, M. A.: Bilirubinemia and Bromsulphalein Retention. Proc. Soc. Exper. Biol. & Med. 34: 467, 1936.

12. Tagnon, N. J., Robbins, G. F., and Nichols, M. P.: The Effect of Surgical Operation on the Bromsulphalein-retention Test. New England J. Med. 238: 556, 1948.

13. Galt, J., and Hunter, R. T.: The Effect of Aureomycin on Certain Liver Function Tests and Blood Coagulation. Am. J. Med. Sci. 220: 508, 1950.

14. Stefanini, M.: Mechanism of Blood Coagulation in Normal and Pathologic Conditions: Am. J. Med. 14: 64, 1953.


174

15. de Takats, G., and Marshall, M. H.: The Response of the Clotting Equilibrium to Postoperative Stress. Surgery 31: 13, 1952.

16. Fahey, J. L., Ware, A. G., and Seegers, W. H.: Stability of Prothrombin and Acglobulin in Stored Human Plasma as Influenced by Conditions of Storage. Am. J. Physiol. 154: 122, 1948.

17. Hidalgo, J., Fowell, A. H., and Rolls, R. I.: The Effect of Tissue Damage on the Plasma Fibrinogen Level. Surg. Gynec. & Obst. 95: 661, 1952.

18. Lawler, A. L., and Hirst, R. R.: The Hanger Cephalin Cholesterol Flocculation Test and the Maclagan Thymol Turbidity Test. U. S. Armed Forces Med. J. 1: 902, 1950.

19. Rappaport, A. M., Clark, D. W., and Stewart, M.: The Effect of Liver Ischemia on Plasma in the Dog, as Measured by the Electrophoretic Analysis. Proc. Soc. Exper. Biol. & Med. 80: 585, 1952.

20. Chanutin, A., Hortenstine, J. C., Cole, W. S., and Ludwig, S.: Blood Plasma Proteins in Rats Following Partial Hepatectomy and Laparotomy. J. Biol. Chem. 123: 247, 1938.

21. Hanger, F. M.: Serological Differentiation of Obstructive from Hepatogenous Jaundice by Flocculation of Cephalin-cholesterol Emulsions. J. Clin. Invest. 18: 261, 1939.

22. Geller, W., and Tagnon, M. J.: Liver Dysfunction Following Abdominal Operation, the Significance of Postoperative Hyperbilirubinemia. Arch. Int. Med. 86: 908, 1950.

23. Crosby, W. H. and Howard, J. M.: The Hematologic Response to Wounding and to Resuscitation Accomplished by Large Transfusions of Stored Blood. A Study of Battle Casualties in Korea. Blood 9: 439, 1954.

24. Cantarow, A., Wirtz, C. W., Snape, W. J., and Miller, L. I.: Excretion of Bilirubin and Bromsulphalein in Bile. Am. J. Physiol. 154: 211, 1948.

25. Beecher, H. K., Burnett, C. H., Shapiro, S. L., Fiorindo, A. S., Smith, L. D., and Eugene, R. S.: The Physiologic Effect of Wounds. Surgery in World War II. Office of The Surgeon General, 1952.

26. Cantarow, A., and Wirtz, C. W.: The Effect of Dog's Bile, Certain Bile Acids and India Ink on the Bilirubinemia and the Excretion of BSP. Am. J. Digestive Dis. 10: 261, 1943.

27. Duesberg, R.: Biologic Relations of Hemoglobin in Normal and Pathologic Conditions. Arch. Exp. Path. & Pharmacol. 174: 305, 1934.

28. Gray, H., and Lunt, L. K.: The Effect of Hemorrhage before and after Exclusion of Abdominal Circulation, Adrenals, or Intestines. Factors Affecting the Coagulation Time of Blood. Am. J. Physiol. 33: 332, 1914.

29. Berquist, G.: Changes in Blood in Connection with Thromboembolism. Acta chir. Scandinav. (Supp. 101) 92: 132, 1945.

30. Chute, A. L.: Changes in Liver Function during Shock. Symposium on Shock, Army Medical Service Graduate School, May 1951.

31. Howard, J. M.: The Metabolic Response of the Battle Casualty. To be published.

32. Snyder, H. E., Snyder, C. D., and Bunch, L. D.: Serum Cholinesterase Levels in Surgical Patients. Am. Surgeon 17: 959, 1951.

33. Frawley, J., Artz, C. P., and Howard, J. M.: Plasma Cholinesterase in the Battle Casualty. To be published.

34. Frawley, J., Howard, J. M., and Artz, C. P.: Protein Metabolism after Injury. To be published.


175

Appendix

Abbreviations, Definitions and Symbols

    A. Trauma

      1. Grading of Trauma

        a. A minimally wounded man is a casualty who does not require blood, has wounds of a degree requiring limited débridement usually under local and rarely general anesthesia.

        b. A lightly wounded man is a casualty with less than five trauma points (see point system) who may or may not require small transfusions and rarely has suffered from shock.

        c. A moderately wounded man is a casualty with 5 to 10 points; he probably has suffered some degree of shock and usually requires 2,500 to 5,000 ml. of blood.

        d. A severely wounded man is a casualty with more than 10 points; he has almost certainly been in shock and usually receives more than 5,000 ml. of blood during the first 24 hours.

      2. Location of Trauma

        a. Hepatic wounds include any penetrating wounds of the liver without reference to size or extent of injury.

        b. Abdominal wounds include all wounds in which the peritoneum is penetrated excepting those wounds in which the liver is also involved.

        c. Peripheral wounds include all other wounds of the body including chest wounds.

    B. Shock It is extremely difficult, if not impossible, to arrive at a classification of shock which is acceptable to all clinicians. It is important, however, that the readers of this report have an understanding of our grading of shock. Even in this classification not all the patients fulfill all the criteria for any one shock group. For the purpose of discussion or analysis, it is necessary that each patient be placed in the group that he most closely fits. After careful consideration of the patients in this series, each was placed in one of the following groups using the criteria outlined below.

      1. No Shock Group

        a. Systolic blood pressure above 100 mm. Hg.

        b. Skin color, normal

        c. Skin temperature, normal


176

        d. Degree of constriction of the conjunctival vessels, normal

        e. Nail beds, rapid and complete filling

      2. Moderate Shock Group

        a. Systolic blood pressure usually between 80 and 100 mm. Hg.

        b. Skin color, usually but not invariably blanched.

        c. Skin temperature, occasionally but not usually reduced

        d. Degree of constriction of the conjunctival vessels usually moderate

        e. Nail beds, usually fill with reduced speed but do fill completely.

      3. Severe Shock Group

        a. Systolic blood pressure usually below 80 mm. Hg.

        b. Skin color: invariably some degree of, and usually marked, blanching

        c. Skin temperature, usually but not invariably reduced

        d. Degree of constriction of conjunctival vessels: universally some degree of, and usually marked, constriction

        e. Nail beds, universally filling, impaired to some degree and usually to a marked degree

        f. Peripheral veins almost invariably have poor filling and venipuncture is difficult.

        g. Response to transfusion: usually slow

    Point System*

      A. Purpose. This system of tabulating "total trauma points" was devised so that patients with varying degrees of trauma could be compared graphically.

      B. Method of Tabulating. In arriving at the total points a given casualty should receive for his injury, the injury itself, duration of injury, and response to therapy are considered.

        1. Injury-magnitude and location

          a. Simple penetration wounds of the chest or abdomen-1 point

          b. Fractures of the femur or pelvis-2 points

          c. Fractures of any other bone-1 point

          d. Soft tissue injury-1 point per "hand" of traumatized tissue (one hand represents the amount of tissue the size of the clenched fist)


*Prepared in conjunction with Lt. Michael Ladd, MC

 


177

          e. Amputations

            1. Ankle or wrist-1 point

            2. Calf, supracondylar and upper arms-2 points

            3. Middle and upper thigh-3 points

          f. Visceral injury

            1. 1 point for each of the following: penetrating wounds of the stomach, duodenum, spleen, diaphragm, lungs, small intestine (less than 4 penetrations), large intestine (1 perforation) and bladder

            2. 11/2 points for lacerations of the kidney and 2 points for nephrectomy

            3. 1 to 3 points for laceration of the liver (given in proportion to the extent of injury)

            4. 2 to 3 points given for multiple perforations of the small and large intestines (given in proportion to the extent of injury)

      2. Duration of injury-1 point was given for each 2-hour duration of injury before the patient was admitted to the MASH

      3. Response to therapy with blood, plasma or albumin-1 point for each 5 units of intravenous therapy needed to resuscitate the patient.

    C. Case Presentation for Tabulation of Trauma Points. The patient was admitted to the MASH 4 hours after injury. Two units of plasma had been given in the forward area. Fifteen units of blood were required to complete operation. The patient was found to have-

 

Points

1. Penetrating wound of the chest without injury to the lung

1.0

2. Penetrating wound of the abdomen

1.0

3. Massive injury to liver

3.0

4. Laceration of the spleen

1.0

5. Three penetrations of the small intestine

1.0

6. Left supracondylar amputation

2.0

7. Six penetrating wounds of the lower extremity probably involving about one and one-half "hands" of damaged tissue


1.5

    15 units of blood

3.0

    2 units plasma

0.4

    4 hours duration

2.0

 

Total


15.9

Return to Top