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Chapter X

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

Gallbladder Function (Cholecystographic Studies) Following Nonspecific Trauma*

Captain John M. Howard, MC, USAR

Studies by the Surgical Research Team in Korea demonstrated that the response to severe trauma is a response of every system and every organ in the body. As a generalization, this response persists for days or weeks; the duration often appearing proportional to the magnitude of the original injury.

As part of this study of the response of various organs to non-specific trauma, the ability of the gallbladder to concentrate various radio-opaque media was observed.

Materials and Methods

The observations were made on young male subjects, 18 to 25 years old, who had been healthy until wounded in battle. Casualties were selected with degrees of trauma which varied from minimal injuries which could be débrided under local anesthesia to severe injuries which threatened the soldier's life. No casualty was included who had direct trauma to the gallbladder and only one was included who had a direct injury to the liver. Two other soldiers, one with acute appendicitis and one with a strangulated hernia, volunteered to take part in the study and were included. Noncombat soldiers served as controls.

Three contrast media were used separately; Iodeikon (sodium tetraiodophenolphthalein) 3.5 grams orally or intravenously, Telepaque (3-ammo-2,4,5-triiodophenyl)-2-ethyl propionic acid), 3.0 grams orally, and Priodax (beta (4-hydroxy-3,) (5-diiodophenyl) alpha-phenyl-propionic acid), 3.0 grams orally.

Following ingestion of the opaque medium, the patient fasted until the study was completed. Roentgenograms were made between 8 and 24 hours after taking the drug. When feasible, serial exposures were made.

Results

Three healthy soldiers served as controls, and six separate cholecystograms were made utilizing separately all three drugs.


*Previously publisbed in Surgery 36: 1051, 1954.


192

Without exception, roentgenograms, made between 12 and 16 hours after the subject took the drug, revealed a clearly defined gallbladder. In two instances, the density of the gallbladder was somewhat less than in the others but the resultant shadow was distinct.

Twenty-two patients were studied during the first 10 days after injury. Most of them were first studied within 3 days after injury. When feasible, the study was repeated one or more times before the patient was evacuated.

The results of the study are summarized in Table 1. With few exceptions, the gallbladder could not be visualized by cholecystography. It could not be visualized in individuals who suffered injury to the brain, chest, abdomen, extremities and after inguinal herniorrhaphy for an incarceration of the small bowel. Nonvisualization was noted in one burned patient who had not received anesthesia. Other casualties had received spinal, inhalation anesthesia (nitrous oxide, oxygen, ether), or pentothal. During the first week after injury, the gallbladder was visualized in only three patients. Five patients were studied after a lapse of 8 to 10 days following injury; visualization was noted in only two of these patients.

Of the five patients whose gallbladder was visualized roentgenographically at some time during the study, none had an intra-abdominal injury. One patient with a minor wound of the scalp which was repaired under local anesthesia appeared to have normal gallbladder function on the following day. Conversely, the gallbladder of Patient Q was demonstrated only on the eighth day after injury and after three previous studies had failed to demonstrate the gallbladder.

Discussion

The reason why the gallbladder cannot be visualized after injury is not apparent. It cannot be explained on an anatomical basis although injuries to the extremities appear to have somewhat less effect. Abdominal injury is not a prerequisite for this response. Anesthesia is apparently not the cause for this abnormality as one patient received no anesthesia and the anesthetic agent and route of administration varied from patient to patient.

Failure of Hepatic Excretion

One of the possible reasons for non-visualization might be a failure of the liver to excrete the contrast media. Hepatic function studies were done on six of these patients as well as many other casualties. Bromsulphalein retention (45 minutes after injection of 5.0 mg. per kg. of body weight) often reached 20 to 30 per cent on the day after


193

Table 1. Results of Cholecystographic Studies

Patient

Injury

Day Post-injury

Drug

Route

Hours after Dye

Roentgenographic Result

A

Normal

---

Iodeikon

Oral

12
16

Visualization
Visualization

A

Normal

---

Iodeikon

Intravenous

8
12

Hazy visualization
Clear-cut visualization

A

Normal

---

Priodax

Oral

11
16

Clear-cut visualization
Clear-cut visualization

A

Normal

---

Telepaque

Oral

14

Clear-cut visualization

B

Normal

---

Telepaque

Oral

14
16

Clear-cut visualization
Clear-cut visualization

C

Normal

---

Priodax

Oral

15

Visualization

D

Perforation of lung

4

Iodeikon

Intravenous

10
15
20

Non-visualization
Non-visualization
Non-visualization

E

Traumatic amputation of hand, multiple fractures of lower extremities

4

Iodeikon

Intravenous

12
18
24

Non-visualization
Non-visualization
Non-visualization

F

Penetrating wound of the brain

8

Iodeikon

Intravenous

12
15
21

Non-visualization
Non-visualization
Non-visualization

G

Strangulated inguinal hernia

1
3
6

Iodeikon

Intravenous
Intravenous
Oral

12
12
12

Non-visualization
Non-visualization
Non-visualization

H

Perforation of abdominal wall

1

Iodeikon

Intravenous

13
16

Non-visualization
Non-visualization


194-195

Table 1. Results of Cholecystographic Studies-Continued

Patient

Injury

Day Post-injury

Drug

Route

Hours After Dye

Roentgenographic Result

I

Laceration of scalp. Repaired under local anesthesia.

1

Iodeikon

Intravenous

13

Clear-cut visualization

J

Perforation of lung and liver

5

Iodeikon

Oral

12

Non-visualization

K

Evisceration 2 days after colostomy and repair of jejunum

4

7
10

Iodeikon

Iodeikon
Iodeikon

Intravenous

Intravenous
Oral

8
21
13
13

Non-visualization
Non-visualization
Non-visualization
Non-visualization

L

Multiple penetrating wounds of soft tissue

3

Iodeikon

Intravenous

14

Non-visualization

M

Penetrating wounds of the chest

3
5

Iodeikon
Iodeikon

Intravenous
Intravenous

11
12

Non-visualization
Non-visualization

N

Bilateral perforation of kidney

2

3

Iodeikon

Iodeikon

Oral

Oral

12
36
7

Non-visualization
Non-visualization
Non-visualization

O

Perforation of lung

1
2

Iodeikon
Iodeikon

Oral
Oral

6
6
18

Non-visualization
Non-visualization
Non-visualization

P

Second and third degree burns of face, neck, hands. No anesthesia except demerol

12 hours after injury
2

Iodeikon

Iodeikon

Oral

Oral

11

12

Non-visualization

Non-visualization

Q

Retroperitoneal penetration

1
4

8

Iodeikon
Iodeikon
Iodeikon
Iodeikon

Oral
Oral
Oral
Intravenous

17
19
19
14

Non-visualization
Non-visualization
Non-visualization
Clear-cut visualization

R

Acute appendicitis, appendectomy

1

Iodeikon

Oral

6
26

Non-visualization
Non-visualization

S

Perforation of thigh, bilateral. Severance of femoral vein, frostbite of feet

2

Telepaque

Oral

12
15

Non-visualization
Non-visualization

T

Traumatic amputation of leg

5

10

Telepaque

Telepaque

Oral

Oral

14
17
15

Non-visualization
Non-visualization
Clear-cut visualization

U

Shattering fracture of humerus and scapula. Large soft tissue defect

5

8

Telepaque

Telepaque

Oral

Oral

14
17
14

Non-visualization
Non-visualization
Non-visualization

V

Perforation of popliteal artery, minor soft tissue wounds

2

Telepaque

Oral

16

Clear-cut visualization

W

Traumatic amputation of foot and hand

5

Telepaque

Oral

14

Visualization

X

Traumatic amputation of thigh

3

5

Telepaque
Telepaque
Telepaque
Telepaque

Oral
Oral
Oral
Oral

16
20
14
17

Non-visualization
Non-visualization
Non-visualization
Non-visualization

Y

Perforation of knee, thigh, neck and face

3

5

Telepaque

Telepaque

Oral

Oral

14
18
17

Non-visualization
Non-visualization
Non-visualization


196

the injury; gradually falling to normal during the ensuing week.1 In two of the six patients in this series who had both studies, the gallbladder remained "non-functioning" after the bromsulphalein excretion had returned to normal. Furthermore, Bockus2 found that gallbladder visualization persisted in the face of hepatic disease until the bromsulphalein retention reached 25 per cent or more after 30 minutes.

In this group of casualties, the plasma bilirubin concentration rose during the first 24 hours, often reaching 2.0 to 3.0 mg. per 100 cc. It then tended to fall toward normal. In the group studied with cholecystograms, three had plasma bilirubin determinations performed; again this hepatic function returned to normal before the gallbladder could be visualized by cholecystography. Furthermore, Readinger and his associates3 showed that in patients with viral hepatitis, the gallbladder could still be visualized roentgenographically until the plasma bilirubin concentration reached approximately 11 mg. per 100 cc.

Failure of Gastrointestinal Absorption

Although this may be a factor of some importance, it is not the basic cause of non-visualization as demonstrated by the failure to visualize the gallbladder following intravenous administration of the drug.

Primary Failure of Gallbladder Function

This is apparently the cause of non-visualization of the gallbladder by cholecystography following injury. There is reasonable evidence to support the hypothesis that the gallbladder, embryologically a part of the gastrointestinal tract, takes part in the paralytic ileus following injury. A failure of the gallbladder to empty, and thus to receive fresh hepatic bile containing the contrast medium, might be one factor; another might be a decreased absorption of water from the bile and thus a failure to concentrate the drug sufficiently to permit roentgenographic visualization. There is ample evidence to demonstrate both factors at play in the gastrointestinal tract. Clinical experience has amply demonstrated that a degree of paralytic ileus follows any severe trauma and may be prolonged after injury of abdominal viscera. Studies with deuterium oxide (heavy water) have demonstrated that the absorption of water from the gastrointestinal tract is delayed following trauma. This defect in absorption may persist for as long as a week following the return of "clinically normal" gastrointestinal function.4

The fundamental cause of such a gallbladder defect is unknown. Gallbladder motility is under the hormonal control of cholecystokinin.2


197

There is no evidence that the motility of the gallbladder in the human is under the direct influence of the autonomic nervous system. The release of epinephrine, as part of the response to trauma, could hardly be the explanation as Stewart,5 in the early days of cholecystography, routinely administered epinephrine coincident with the intravenous injection of the cholecystographic drug in order to minimize reactions from the latter drug. The effect of adrenal cortical hormones on cholecystic function has not yet been determined.

Radiologists and clinicians have occasionally made related observations. Skinner6 described four patients with subacute perforations of gastroduodenal ulcers whose gallbladder could not be visualized roentgenographically, whereas 30 patients with chronic ulcers had normal gallbladder function. He hypothesized that intra-abdominal disease which resulted in signs of peritoneal irritation was associated with non-visualization. Leb7 also noted that numerous patients with duodenal ulcer had non-visualization of the gallbladder following the intravenous administration of the drug. Of 25 patients with duodenal ulcer and non-visualization, 10 were found to have an entirely normal gallbladder. He postulated that a "nervous irritation of all intra-abdominal organs" resulted from the ulcer.

Isolated reports include mention of non-visualization associated with acute appendicitis, perforated ulcer, and other acute abdominal disease.8, 9

Silvani and McCorkle10 reported that of 28 patients with acute pancreatitis, 16 had a failure of gallbladder visualization following the intravenous administration of Iodeikon. At least 11 of the latter 16 patients subsequently proved to have a normal gallbladder. Non-visualization occurs frequently during the late months of pregnancy.11

Boyden12 noted that stimulation of the gastrointestinal tract, particularly of the cecum, produced inhibition of gallbladder motility.

Rewbridge and Halpert13 reported that following the operative injection of lipiodol into the gallbladder of the dog, the oil often remained in the gallbladder for several days. Patients on a fat-free diet have been reported to develop a physiological stasis of gallbladder bile. Non-visualization of the gallbladder may result.14, 15

Conclusions

Following severe injuries to any part of the body, cholecystography frequently resulted in a temporary non-visualization of the gallbladder. This evidence strongly suggests that the gallbladder participates in the body's response to injury.


198

References

1. Scott, R., Olney, J. M., and Howard, J. M.: Hepatic Function of the Battle Casualty. Report to the Army Medical Service Graduate School, 1954 (Chapter 8 of this volume).

2. Bockus, H. C.: Gastroenterology, Vol. III. W. B. Saunders Co., Philadelphia, 1946.

3. Readinger, H. M., Swift, W. E., Gardner, H. T., and Sheedy, J. A.: Oral Cholecystography in Patients with Viral Hepatitis. Am. J. Medicine 8: 611, 1950.

4. Howard, J. M.: Absorption of Water (Deuterium Oxide) from the Gastrointestinal Tract Following Injury. Report to the Army Medical Service Graduate School, 1954.

5. Stewart, W. H.: Further Experiences with Tetrabromphenolphthalein Sodium Salt in the Roentgenographic Diagnosis of Gallbladder Disease. Am. J. Roentgen. 13: 259, 1925.

6. Skinner, E. H., Lockwood, I. H., and Deweese, E. R.: The Failure of Cholecystographic Filling in the Presence of Acute Pyloric Pathology. Am. J. Roentgen. 19: 340, 1928.

7. Leb, A.: An Experimental Contribution to the Negative Cholecystographic Response in the Presence of Duodenal Ulcer. Fortschr. a. d. Geb. d. Roentgenstr. 44: 16, 1931. Abstracted by Jarre, H. A.: Radiology 17: 1004, 1931.

8. Hawley, S. M.: Comparison of Intravenous and Oral Cholecystography. Am. J. Roentgen. 26: 232, 1931.

9. Jordan, S. M.: Correlation of Gastroenterology and Surgery. J. A. M. A. 138: 791, 1948.

10. Silvani, H. L., and McCorkle, H. J.: Temporary Failure of Gallbladder Visualization by Cholecystography in Acute Pancreatitis. Ann. Surg. 127: 1207, 1948.

11. Levyn, L., Beck, E. C., and Aaron, A. H.: Further Cholecystographic Studies in the Late Months of Pregnancy. Am. J. Roentgen. 30: 774, 1933.

12. Boyden, E. A., quoted by Mooney, A. C.: Cholecystography. A Review in Full. British J. Radiol. 8: 403, 1935.

13. Rewbridge, A. E., and Halpert, B.: Roentgen-Physiological Studies of the Gallbladder. Am. J. Roentgen. 24: 634, 1930.

14. Brewer, A. E.: Physiological Stasis: A Cause of Cholecystographic Error. Am. J. Roentgen. 58: 106, 1947.

15. Curl, H.: High Fat Diet Preceding Cholecystography; Review of Literature and Experimental Studies on Filling Normal Gallbladder. J. A. M. A. 119: 607, 1942.