Medical Science Publication No. 4, Volume 1
FATIGUE AND METABOLIC DEFICIT
A STUDY OF THE COMBAT AND INJURED SOLDIER*
JOHN M. HOWARD, M.D.
These observations were made on the Eastern Front in Korea during thefirst half of 1952 and to a lesser extent throughout the succeeding year.January 1952 was a time when the front lines had begun to stabilize. Therewas complete uncertainty among the troops as to the tactical moves to bemade by our forces as well as the forces of the enemy. Fighting was beginningto be limited to probing actions, patrols, and exchange of mortar and heavyartillery fire. The front lines were strung out across a chain of mountaintops and men had, at this time, reasonable protection from the cold.
Under these conditions, fatigue was seldom due to physical hardships.Fatigue was due to continued emotional stress-and, I believe, in part touncertainty. This is the fatigue which does not disappear with sleep, andwhich has a cumulative effect. Under the conditions of 1952 in Korea, theextreme form, combat fatigue, was seldom recognized.
The question arose: Does the stress of combat lead to adrenal corticalinsufficiency? Our studies permit a generalization only to the conditionsin Korea. The studies were made under conditions of chronic stress, andI use the term deliberately, for I believe that it is the method or weaponby which strong men are being broken in certain parts of the world today.
The studies, obviously, had to be made in the front lines. They representwhat can be achieved for the mutual welfare of our troops when problemsare explained and approached on a cooperative basis.
Our primary aim was to get complete 24-hour urine collections from troopsunder combat stress. With the cooperation of the Army surgeon, the corpsand division surgeons and the Commanding General of the infantry division,our officers and men gained access to the front lines to live and to workwith the combat troops. Volunteers, including the company officers, wereobtained because of their respect for the cooperating battalion surgeonsand their corpsmen.
*Presented 19 April 1954, to the Course on Recent Advances in Medicine and Surgery, Army Medical Service Graduate School, Walter Reed Army Medical Center, Washington, D. C.
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Cooperation seemed complete. The completeness of the urinary collectionswas roughly checked by comparing the volume and the specific gravity.
Aliquots of the collection of urine were preserved in toluene or byrefrigeration and shipped to the Department of Biochemistry here at theArmy Medical Service Graduate School for analysis of 17-ketosteroids andcorticosteroid content. The methods of analysis have been previously describedand consisted of modifications of the Zimmerman and formaldehydogenic methods.(1)
Noncombat soldiers served as controls. The excretion of steroids indicatednormal function as indicated by examples in table 1.
Three groups of combat troops were studied. They represented differentgroups under somewhat varying tactical conditions between January and July1952. An effort was made to obtain approximately 12 volunteers in eachgroup and to study each man for three consecutive days.
The results of individual studies are demonstrated in figures 1 to 6.
Table 1. Excretion of Steroids
Subject | Day | Urine volume, cc. | 17-ketosteroids | Corticosteroids |
No. 1 | 1 | 750 | 15. 1 | 1. 4 |
No. 1 | 2 | 800 | 19. 0 | 0. 9 |
No. 1 | 3 | 740 | 16.6 | 2. 4 |
No. 2 | 1 | 700 | 10. 9 | 1. 6 |
No. 2 | 2 | 600 | 11. 1 | 1. 7 |
No. 2 | 3 | 600 | 10. 5 | 1. 5 |
Average of 4 subjects |
|
|
|
|
Reported normal range | ---------------------------- | ------------------------------------- | 8. 0-22. 0 | 0. 6-2. 6 |
A correlation between the external environment and the steroid excretionis not always possible but table 2 indicates that the adrenal responsewas noted fairly uniformly throughout a group during the same period oftime. These soldiers had all been under daily fire for 40 days. On thefirst day of the study, they were under an unusually heavy barrage. Ofthe 12 men studied that day, only 1 had a corticosteroid excretion whichwas normal. All the others were elevated. Four had an excretion increasedto almost 400 percent of normal. The following day, the artillery and mortarfire tapered off and so did the adrenal response. The next 2 days werequiet so that on the fourth day, the steroid excretion had, without exception,subsided to normal.
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This trend is best demonstrated by the average values shown in table3. The 17-ketosteroid excretion was normal throughout this period.
Three soldiers shared a bunker which was in the center of the activity(fig. 1). Their bunker was destroyed by mortar fire a few hours after the24-hour period ended and one of the soldiers was killed. Each demonstratedan increase to 200 to 300 percent in corticosteroid excretion but eachhad a normal 17-ketosteroid excretion.
Figure 2 demonstrates the gradual decrease in adrenal activity as thestress decreased. The maximal corticosteroid excretion did not
FIGURE1. Demonstrating the response of three men whoshared the same bunker on the day it was destroyed by incoming mortar fire.These men had been on front line duty for 40 days.This represents the adrenalresponse to acute emotional stress after 40 days of exposure. The corticosteroidexcretion is elevated to 200 to 300 percent of normal. The 17-ketosteroidexcretion is normal.
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always coincide with the heaviest fire (fig. 3) but, if not, followedshortly thereafter. Adrenal cortical response continued for 24 hours afterthe shelling had subsided (fig. 4). The adrenal response to the stressof battle appears comparable to the response of major injuries as demonstratedby figure 5. There can be no doubt that these men were under stress andthat their adrenal cortex remained responsive.
A total of 35 combat soldiers were studied by this method. The excretionof 17-ketosteroids was normal. The excretion of corticosteroids was normalor elevated. The increase in excretion could usually, but not always, becorrelated with the day's activity. In no instance was evidence of adrenalinsufficiency detected.
In a different phase of the study, an officer under long-standing nervoustension was found to be developing an anxiety state which was
FIGURE2. Demonstrating a subsidencein the adrenal cortical response in this soldier in the face of continueddanger.
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Table 2. Combat Stress*-Corticosteroid Excretion**by Combat Soldiers, Milligrams per 24 Hours
Date | Activity | 1 | 2 | 3 | 4 | 5 | 6 | 7 | 8 | 9 | 10 | 11 | 12 | 13 | 14 | 15 |
11 May 1952 | Heavy artillery fire | 3.9 | 6.2 | ---- | 5.3 | 5.9 | 5.0 | 5.5 | ---- | 9.4 | 4.9 | 8.6 | 8.6 | 2.6 | ---- | 9.2 |
12 May 1952 | Fewer incoming shells | 6.3 | 2.1 | 4.4 | 6.2 | ---- | ---- | 3.1 | 4.5 | 4.3 | ---- | ---- | ---- | 1.0 | 1.6 | ---- |
13 May 1952 | Rain-quiet | ---- | ---- | ---- | ---- | ---- | ---- | ---- | ---- | ---- | ---- | ---- | ---- | ---- | ---- | ---- |
14 May 1952 | Quiet day | 2.0 | 2.1 | 1.0 | 1.5 | ---- | ---- | 2.0 | 2.1 | 1.1 | 1.2 | ---- | 1.0 | 1.0 | 1.1 | ---- |
*All men on front line for previous 40 days.
**Normal 0.6-2.6 mg. per day.
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becoming incapacitating. After 30 days of increasing tension, his corticosteroidexcretion was found to be high (fig. 6). Adrenal insufficiency was notan associated factor.
The next step was to study the wounded man to determine if he couldmanifest the normal adrenal cortical response to physical injury. Thiswas approached in two ways.
FIGURE3. After 40 days of exposure,this officer responded to an increased hazard by an increase in excretionof corticosteroids. The 17-ketosteroid excretion remained normal.
First, 64 casualties were studied with eosinophile counts immediatelyafter injury. Each demonstrated a typical adrenal cortical response asmanifested by a marked depression in the concentration of circulating eosinophiles(1).
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An additional 20 casualties were selected for continued study duringthe day of injury and the succeeding 7 to 14 days thereafter (1).
TABLE 3.Combat Stress-All Men on Front Line 40 Days-A Study of 15 Soldiers
Date | Activity | Average corticosteroid excretion* milligrams per24 hours |
11 May 1952 | Heavy artillery fire | 6.3 mg. |
12 May 1952 | Fewer incoming shells | 3.7 mg. |
13 May 1952 | Rain-quiet | ----- |
14 May 1952 | Quiet day | 1.5 mg. |
*Normal range 0.6-2.6 mg.
FIGURE4. Demonstrating a continuedresponse for 24 hours after the shelling had subsided.
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FIGURE5. The response to danger appears approximatelyequal to the response to major injury in these specific instances. Bothsubjects demonstrate fairly representative findings.
The following two patients are typical of the group.
Patient No. 6
Twenty-one-year-old American soldier, weight 175 pounds, blood typeA, in Korea for 30 days and in combat 20 days. This soldier was woundedby multiple shell fragments at 0330 hours, 3 August 1952. Arriving at thebattalion aid station 1 hour later, he was given 15 mg. of morphine, 600,000units of penicillin, and 0.5 cc. of tetanus toxoid. On arrival at the hospital5 hours after injury, his blood pressure was 148/78 and his pulse rate104 per minute. He was pale and considered to be in incipient shock. After1,500 cc. of blood in the preoperative ward, his pressure was 160/100.His wounds included a perforation
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of the right side of the chest, diaphragm, and liver. The wound of theright lobe of the liver would easily admit four fingers. In addition, hehad multiple small penetrating wounds of three extremities.
FIGURE6. This officer had not been under condition ofcombat nor actual personal danger. Nervous tension became as intense asin soldiers in the front lines. Adrenal function appears to be increasedduring a representative period of time and activity.
A laparotomy was performed and the hepatic wound drained. The soft tissuewounds were débrided. Ether, oxygen, and nitrous oxide were givenby inhalation. His operative course was smooth, his pressure ranging about120/75, pulse 120. Another pint of blood was given during operation. Thoracentesiswas repeatedly performed postoperatively until on the fifth day a tubedrainage of the right side
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of the chest was performed. Blood loss was estimated at 500 cc. duringoperation. His subsequent course was smooth.
This soldier demonstrated the rise in corticosteroid excretion followinginjury. The response subsided but was detectable again on the seventh day(fig. 7) due, perhaps, to the earlier secondary trauma of intubation ofthe pleural cavity. This patient's sodium intake
FIGURE7. Note the fall in eosinophile concentrationin the blood and the increase in the urinary excretion of corticosteroids.
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was quite limited so that he was slow to develop a positive sodium balance(figs. 8, 9, and 10). The potassium diuresis was rather marked. He, therefore,demonstrated the manifestations of a rather typical adrenal cortical responseto injury (fig. 11).
Patient No. 8
This soldier, 30 years of age, was wounded by mortar shell fragmentsat 1100 hours 20 September 1952. The injuries included traumatic amputationof both legs and both upper extremities at the forearm. He was seen shortlythereafter at the battalion aid station where he was given albumin 500cc., morphine 30 mg., streptomycin 1.0 gram, and penicillin 600,000 units.He arrived at the hospital 2.5 hours after injury. At this time, his bloodpressure could not be measured because of the limited areas exposed. Hispulse rate was 102 per minute. He was pale, lethargic and dry. No peripheralvessels were visible.
Eighteen pints of blood were given intra-arterially. Meanwhile, hemostasiswas obtained. The pulse averaged 130 to 140 beats per
FIGURE8. Sodium intake was zeroduring the first 2 days so that he was slow to develop a positive sodiumbalance. Potassium diuresis was marked. Figure above column representsintake, figure in column represents output, and figure below column (andshaded area) represents balance (after Moore).
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CUMULATIVE SODIUM AND POTASSIUM BALANCE (Meq.)
minute and was irregular. At 2000 hours, under pentothal, oxygen andether anesthesia, four surgical teams reamputated all four extremities.The operation required only 20 minutes but was poorly tolerated. By theend of surgery the patient had received 23 pints of blood in addition to5 units of albumin. The following day he received three more pints of blood.His subsequent convalescence was fairly slow but uneventful.
His wounds were dressed on the sixth postoperative day. No anesthesiawas used at this time.
Figure 12 demonstrates the rise in corticosteroid excretion on the dayafter injury. This response slowly subsided but was again noted
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after the trauma of the secondary dressing on the sixth day. The 17-ketosteroidexcretion remained essentially normal. Potassium diuresis and sodium andwater retention (figs. 13, 14, 15, 16) were uniformly observed.
These patients were rather typical of the group. Again, each of the20 patients demonstrated a normal response of the adrenal cortex followinginjury.
FIGURE10. Note the evidence of sodium retention andpotassium loss as indicated by the rapid decrease in the Na/K ratio.
Summary
A study of the combat casualty was made during the first half of 1952on the Eastern Korean front. Adrenal cortical function appeared normalin the front line soldiers. After prolonged exposure to the stress of battleexposure, acute danger stimulated an adrenal response of the magnitudefound after severe combat injury.
Following combat injury, each soldier studied demonstrated a responseof the adrenal cortex.
Under the conditions of the study in Korea, therefore, adrenal insufficiencywas not found to result from combat stress.
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Reference
1. Howard, J. M., Olney, J. M., Frawley, J. P., Peterson,R. E., Serfin, Guerra, and Dibrell, W.: Studies of Adrenal Function inthe Combat and Wounded Soldier. Report to the Army Medical Service GraduateSchool, 1954.
DAILY WATER BALANCE (c.c.)
NO CORRECTION FOR INSENSIBLE LOSS
FIGURE11. Demonstrating a positivewater balance for at least the first few days.
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FIGURE12. The corticosteroid excretion was elevatedon the day after injury and thereafter gradually returned to normal. Itagain increased following secondary trauma on the sixth day. The 17-ketosteroidexcretion (normal 8 to 22 mg.) remained essentially normal.
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FIGURE13. Sodium retention was marked throughout thefirst 9 days. Potassium was lost for 2 days and then conserved. Figureabove column represents intake, figure in column represents output, andfigure below column (and shaded area) represents balance (after Moore).
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FIGURE14. Demonstrating the continuingchange.
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FIGURE15. Potassium was excretedin larger amounts than sodium throughout the first week.
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FIGURE16. Demonstrating water retentionearly.