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

A Survey of Plasma Electrolyte Changes in the Seriously Injured Battle Casualty*

Captain John M. Howard, MC, USAR
First Lieutenant John P. Frawley, MSC, USAR
and
Lieutenant Colonel Curtis P. Artz, MC, USA

With the Technical Assistance
of
Joe C. Meikrantz

The explosion of a land mine which avulses a leg or the perforation of the leg by a shell fragment does not result in only a local wound. Although tissue destruction is primarily a local wound, the loss of blood and the absorption of bacterial toxins are at least two concomitant injuries which constitute a wound of the entire organism. Since both the leg and the entire organism are injured, it is not surprising that both respond to the injury in the fight for survival. This response to injury includes a response of every organ, every system, and presumably every cell in the body.

The changes in plasma electrolyte concentrations are not in themselves "dynamic" but are reflections of dynamic changes within the myriad of cells of the many organs, the chief of which is the wound. These changes are believed to represent, in part, the injury and resultant cell degeneration and, in part, the response to the injury and the changes in electrolyte concentrations by living cells.

The magnitude of the total changes in sodium and potassium metabolism following massive injuries of combat soldiers has been demonstrated by balance studies.¹ A 70-kilogram soldier with a gangrenous limb may have a net cumulative loss of 480 milliequivalents of potassium within the first few days after injury. Since the total plasma potassium constitutes only 12 to 14 mEq. and the total extracellular potassium only 60 to 70mEq., a net loss of 480 mEq. represents a shift of intracellular potassium of considerable magnitude. Similarly, casualties conserved as much as 970mEq. of sodium, the equivalent of over 6 liters of normal saline. Plasma concentrations on these patients in the earlier study were determined only at 24-hour

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*This paper is currently being published in Archives of Surgery.

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intervals but occasionally demonstrated striking fluctuations in the early postoperative period. The present study was undertaken to extend the survey of the magnitude of the changes in the immediate period after injury and resuscitation.

In the absence of intestinal obstruction, fistula, or renal failure, most of the serious complications of electrolyte imbalance in the combat casualty will probably be found within the first 24 hours after injury. This hypothesis has not been proved but it is during this period when most of the problems of refractory shock are found, when most of the fatalities occur, and when the most rapid changes in electrolyte concentrations are found. The relationship between refractory shock and electrolyte changes has been strongly suggested by clinical experience² but requires further study.

Materials and Methods

Twenty-five soldiers wounded in combat were selected for study on the basis of the magnitude of their injuries. Studies were begun at the time of admission to the forward surgical hospital and were continued until the patients were evacuated. An effort was made to obtain blood specimens before and after transfusion, immediately after operation, 3, 6, 9, 12,and 24 hours after operation, and daily thereafter. Deviation from the protocol was frequently unavoidable.

Blood was drawn into a dry syringe (Patients No.1 to 17) or a heparinized syringe (Patients No. 18 to 25) and centrifuged; the serum or plasma was separated and immediately frozen in a sealed, hard glass test tube. Sodium and potassium analyses were performed 2 to 3 weeks later. Magnesium analyses were performed several months later after shipment of the frozen specimens to the Department of Biochemistry at the Army Medical Service Graduate School.

For sodium and potassium analyses, samples were selected at random for analysis in groups of 25 or 50, and arbitrary numbers, unassociated with date of admission, were assigned to each patient. All specimens were analyzed by flame photometry, using an internal lithium standard technic. A dilution of 1:200 with 250 ppm lithium was used for sodium determinations and a dilution of 1:25 with 50 ppm lithium for potassium.

Magnesium analyses were performed on eight casualties by the Clayton Yellow method³ which was reproducible within a range of ±0.lmEq./L. in 15 controlled studies. Six healthy soldiers served as controls.

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Controls for the sodium and potassium studies consisted of 20 healthy soldiers. Freezing and storage, under the conditions of the experiment, did not affect the concentration.

Results

The control studies demonstrated an average sodium concentration of143 mEq./L. with a range of 140 to 155 mEq./L. The average plasma potassium concentration was 4.5 mEq./L. with a range of 4.3 to 4.9 mEq./L. The average magnesium concentration was 1.9 mEq./L. with a range of 1.4 to 2.4 mEq./L.

The results of the individual studies are summarized in Table 1. The most striking changes occurred during the first 24 hours. During this period a pattern, although not always found, appeared to evolve. This pattern consisted not only of the well-known fall in sodium concentration but also a definite, transient rise in potassium concentration. Magnesium concentration in the plasma did not appear to follow a predictable pattern but sometimes fell to rather low levels.

Table 1. The Concentration (mEq./L.) of Electrolytes in the Plasma (or Serum) of 25 Severely Wounded Battle Casualties

Patient	Wound Description	Hrs. Postoperative	Plasma
			Na+	K+	Mg.++
No. 1	Penetrating abdominal wound, massive mesenteric damage-15 pts. blood	Preop. 18 42 66 90 114 138 162	mEq./L. 144 137 136 144 134 146 127 125	mEq./L. 4.7 5.3 5.4 4.6 3.4 4.1 4.5 4.9
No. 2	Multiple shell fragment wounds of face, neck, chest, and all extremities-29 pts. blood	10 16 34 58 82 106 130 154	132 127 139 138 120 136 125 102	4.0 6.2 4.2 4.8 5.1 5.1 4.1 3.6
No. 3	Multiple shell fragment wounds of lung, diaphragm, liver, back, both arms	0 16 30 54	135 125 118 120	4.7 4.9 3.7 3.7

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Table 1. The Concentration (mEq./L.) of Electrolytes in the Plasma (or Serum) of 25 Severely Wounded Battle Casualties-Continued

Patient	Wound Description	Hrs. Postoperative	Plasma
			Na+	K+	Mg.++
No. 4	Shell fragment wounds of abdomen, liver, hip, and right leg-47 pts. blood	Preop. 0 15 39 63 87 110 135 158 182 207 231	mEq./L. 139 144 140 136 137 125 125 134 139 125 132 132	mEq./L. 5.0 3.4 6.2 4.5 4.4 3.8 4.0 4.4 4.5 3.9 3.9 3.6
No. 5	Laceration of head, face, penetrating wounds of both thighs and right arm-8 pts. blood	Preop. 0 20 50 94 140 164	137 141 123 130 125 125 132	4.3 5.1 4.8 5.3 4.4 4.9 4.9
No. 6	Shell fragment wounds of cheek, chest, both arms, right leg, fracture of left tibia	Preop. 0 9 33 57 80 104 128 152 178 200 223 247	131 124 131 125 133 134 131 134 141 125 127 120 125	4.8 3.9 4.4 --- 3.9 4.4 4.0 4.2 4.4 5.2 5.1 5.0 4.7
No. 7	Penetrating wound of left hip	Preop. 0 10 34 58	139 141 125 127 116	3.5 4.4 4.4 4.0 3.9
No. 8	Shell fragment wounds of chest and countless small penetrating wounds of entire body-14 pts. blood	20 44 68 92 116	139 123 117 97 109	3.7 6.0 7.5 5.6 5.6

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Table 1. The Concentration (mEq./L.) of Electrolytes in the Plasma (or Serum) of 25 Severely Wounded Battle Casualties-Continued

Patient	Wound Description	Hrs. Postoperative	Plasma
			Na+	K+	Mg.++
No. 9	Shell fragment wound of abdomen, traumatic amputation left leg, multiple penetrations of back-18 pts. blood	Preop. 12 24 48	mEq./L. 144 132 125 125	mEq./L. 5.4 4.6 4.1 3.9
No. 10	Penetrating wound of flank, abdomen and diaphragm	Preop. 0 17	151 125 132	4.7 3.9 4.0
No. 11	Traumatic amputation of leg, multiple wounds of leg and arm-14 pts. blood	Preop. 0 23 47 71	132 129 113 118 116	4.2 4.4 4.9 4.6 4.6
No. 12	Traumatic amputation of foot, penetrating wound of chest, compound fracture of left leg	Preop. 0 18 122 138	146 148 118 128 139	3.6 4.9 4.2 3.0 3.8
No. 13	Penetrating wound of back and abdomen	Preop. 0 24 38	144 144 132 131	4.1 4.7 5.1 4.3
No. 14	Multiple fragment wounds of both legs, arm, fractures of left hand, right arm-8 pts. blood	11 28 52 76 100	132 132 134 134 133	4.0 4.1 4.2 4.3 4.2
No. 15	Multiple wounds of shoulder, back, chest, liver-2 pts. blood	4 10 24 50 74 98 122 146 170	141 141 134 132 134 137 137 137 134	4.3 4.2 4.1 4.1 4.0 3.6 3.5 3.5 4.2
No. 16	Bayonet wound of chest, diaphragm and spleen	3 10 27 51 74	135 137 134 137 134	4.0 5.1 4.2 4.6 4.4

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Table 1. The Concentration (mEq./L.) of Electrolytes in the Plasma (or Serum) of 25 Severely Wounded Battle Casualties-Continued

Patient	Wound Description	Hrs. Postoperative	Plasma
			Na+	K+	Mg.++
No. 17	Multiple wounds of back (involving pelvis and rectum), shoulders and arms	11 18 32 56 80 104 128	mEq./L. 131 132 130 137 134 135 124	mEq./L. 4.0 4.3 4.4 3.9 3.7 3.9 3.5
No. 18	Small arms injury to abdomen, kidney, liver, colon-19 pts. blood. Post-traumatic renal insufficiency	Preop. 3 6 9 12 20	--- 151 --- 141 --- 125	3.8 3.0 3.6 4.2 4.8 5.7	--- 1.30 1.77 --- --- 1.02
No. 19	Traumatic amputation of both legs, multiple wounds of both arms	Preop. OR 0 3	141 153 144 141	3.0 3.2 3.0 3.5	1.42 2.20 1.54 0.83
No. 20	Traumatic amputation at right thigh, perforation of liver, kidney, buttocks. Post-traumatic renal insufficiency	Preop. OR 0 4 7 10 13 37	158 141 146 139 171 155 167 136	3.8 3.7 5.4 6.0 6.3 6.6 5.1 6.6	2.22 2.14 1.82 2.11 1.50 1.97 1.08 ---
No. 21	Multiple shell fragment wounds, massive destruction of muscles of both legs and back-14 pts. blood	Adm. Preop. 0 3 6 9 12 33 57 81 105 129 153	146 155 153 145 145 145 148 137 137 130 136 137 140	3.4 4.5 4.6 5.4 5.9 4.6 4.5 4.6 4.7 3.9 4.3 3.9 4.8	1.75 1.35 1.87 1.52 1.81 1.51 1.67 1.35 1.87 1.42 0.85 1.77 1.63

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Table 1. The Concentration (mEq./L.) of Electrolytes in the Plasma (or Serum) of 25 Severely Wounded Battle Casualties-Continued

Patient	Wound Description	Hrs. Postoperative	Plasma
			Na+	K+	Mg.++
No. 22	Shell fragment wound of left shoulder, fragment lodging in myocardium	Preop. 0 3 6 9 12 24 53 72 101 125 149 173	mEq./L. 144 141 109 147 144 146 137 137 136 132 120 139 138	mEq./L. 4.4 4.4 3.3 4.4 4.3 4.7 5.0 3.7 3.9 3.9 4.2 4.4 4.9	2.03 3.17 2.82 --- 1.17 3.07 0.75 2.08 0.53 2.43 0.89 2.08 1.74
No. 23	Small arms injury of abdomen, involving liver, small and large intestine	0 3 6 9 12 24 48 72 96 120 144 166 192 214 238	158 148 153 148 153 139 141 137 134 139 136 139 137 133 120	4.5 5.1 5.4 5.6 5.7 4.4 4.4 3.5 3.4 3.6 3.6 3.6 4.3 4.2 3.8	--- 1.27 --- --- 1.89 1.89 1.74 1.40 1.45 1.71 1.49 1.36 1.73 --- 1.52
No. 24	Traumatic amputation of right leg, compound fractures of legs, multiple wounds of both buttocks, scrotum, and small intestine-22 pts. blood	Adm. Preop. 0 3 6 9 12 32 56 80 104 128 152 176	132 139 144 141 136 148 127 114 114 116 130 127 137 103	3.7 3.5 4.0 4.8 4.8 4.7 5.1 4.1 3.2 3.3 3.2 3.5 3.6 3.3	1.17 1.75 0.56 1.67 1.34 1.39 1.34 0.82 1.95 1.82 1.52 1.95 --- ---

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Table 1. The Concentration (mEq./L.) of Electrolytes in the Plasma (or Serum) of 25 Severely Wounded Battle Casualties-Continued

Patient	Wound Description	Hrs. Postoperative	Plasma
			NA+	K+	Mg.++
No. 25	Penetrating wound of abdomen, both thighs, compound fracture of right femur-13 pts. blood	Preop. 0 3 6 9 12 21 45 69 93 118 142 166	mEq./L. 144 132 127 141 134 120 125 123 111 123 123 132 132	mEq./L. 4.7 4.9 4.5 4.9 4.2 4.2 4.6 4.2 3.6 4.3 3.6 4.0 4.0	2.08 2.86 2.12 2.66 1.12 2.40 2.92 2.90 2.63 --- 2.08 1.35 2.03

Sodium concentrations fluctuated tremendously during the period of operation and transfusion. Occasionally transfusion was marked by a rise in the sodium concentration but, as a generalization, the fall in concentration was marked and progressive. Patient No. 7 demonstrated a fall from 141 to 125 mEq./L. during the first 10 hours after operation and Patient No. 8 revealed a fall from 139 to 97 mEq./L. within the first 4 days of convalescence although he had no unusual, apparent extra renal loss.

Table 2, demonstrating the average plasma sodium concentration, indicates that the maximal depression was reached on the third day after injury.

The potassium concentration often demonstrated a striking rise during the first 24 hours (Figs. 1 to 6), sometimes increasing by almost 100 percent (Patient No. 4). This period of maximal elevation did not coincide with the period of rapid transfusion and characteristically was associated with no simultaneous potassium intake.

Discussion

The falling sodium concentration coincided with a period of sodium retention by the kidneys¹ and often coincided with a period in which the fluid infusion consisted of normal saline solution, blood (Table 3),

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Table 2. Average Plasma Sodium Levels From 25 Patients at Intervals From Admission to 6 Days Postoperative

	Adm. And Preop.	0-12 Hours Postop.	12-24 Hours Postop.	1 Day Postop.	2 Days Postop.	3 Days Postop.	4 Days Postop.	5 Days Postop.	6 Days Postop.
mEq./L. Na (average)	141	141	133	129	129	125	131	131	133
Number of observations	18	46	22	20	16	13	12	13	10
Per cent of observations below 130 mEq./L.	0%	11%	45%	45%	44%	46%	25%	46%	20%

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FIGURE 1.
Depicting the rising curve of plasma potassium concentration on the day of injury. Note that the elevation
is transient and would have been overlooked had the studies been made at 24-hour intervals only. The plasma
sodium concentration fell from 158 mEq./L. to 139 mEq./L. on the day of injury.
The urinary output remained high throughout the period of study.

FIGURE2.
As in Figure 1, the increasing potassium concentration in the plasma is noted on the day of injury. Within a
period of 32 hours after operation, the plasma sodium concentration fell from 144 mEq./L. to 114 mEq./L.

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FIGURE3.
Within a period of 6 hours, the plasma potassium concentration increased by 50 per cent.

FIGURE4.
This patient with massive wounds and requiring massive transfusions demonstrated an increase
in plasma potassium concentration of almost 100 per cent during the first 15 hours after the completion of operation.

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FIGURE5.
The plasma potassium concentration rose steadily from
the time of admission to the sixth hour after injury.

FIGURE6.
This patient had less tissue destruction but was in profound hemorrhagic shock on admission.
He was not studied intensively during the first 24 hours but thereafter demonstrated a marked and
progressive rise in potassium and fall in sodium concentration.

or dextran, each of which had a sodium concentration approximating that normally found in the plasma. Dilution by infusion was, therefore, not the explanation. The third day post-injury marked not only the maximal average depression in plasma sodium concentration but also marked the time of greatest depression in the serum albumin concentration.⁴

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Table 3. Plasma Electrolyte Concentration (mEq./L.) of Bank Blood Administered to Patients on Day of Injury

Patient	Bottle No.	Na	K	Mg
No. 21	1	148	17.6	1.92
	2	153	18.0	---
	3	148	18.0	1.78
	4	153	17.4	1.10
	5	156	14.8	1.33
	6	171	24.0	0.88
	7	149	13.8	0.38
	8	149	18.4	0.95
	9	146	23.8	---
	10	153	18.8	2.03
	11	153	16.0	2.24
	12	149	15.4	1.50
	13	153	18.8	0.67
	14	145	18.8	0.75
	Average	152	18.1	1.29
No. 24	1	149	18.8	2.14
	2	147	18.0	1.23
	3	149	16.8	1.09
	4	153	15.6	1.33
	5	141	14.0	1.22
	6	153	13.6	1.60
	7	151	13.6	1.22
	8	148	14.0	1.31
	9	160	19.2	2.42
	10	153	19.6	0.70
	11	137	12.8	---
	12	---	---	---
	13	144	15.6	0.32
	14	144	20.4	1.57
	15	141	13.2	1.22
	16	144	15.6	1.34
	17	146	20.0	1.48
	18	148	14.0	1.13
	19	144	23.2	2.49
	20	151	17.6	0.91
	21	146	14.4	1.15
	22	144	18.8	1.33
	Average	147	16.6	1.36

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A few sudden changes deserve special mention. Patient No. 20 showed a rise of plasma sodium from 139 to 171 mEq./L. within a 3-hour period during noradrenalin therapy. His level remained elevated from 155 to 167mEq./L. during 6 additional hours of a slow, continuous noradrenalin infusion. After discontinuing the drug, his concentration dropped to 136 mEq./L.

Another sudden change was noted in Patient No. 22 who received 1,000cc. of dextran (in normal saline) during the first 3 hours following the removal of a shell fragment from his myocardium. During the 3-hour period his plasma sodium concentration fell from 141 to 109 mEq./L. Within another3 hours it returned to the original level.

No interpretation of these marked changes can, as yet, be made.

The rising potassium concentration often found during the first 24 hours after injury and operation coincided with the period of potassium diuresis.¹Only 2 of the 25 patients studied (Patients No. 18 and 20) demonstrated clinically the complication of post-traumatic renal insufficiency. Patient No. 18 showed a rise in potassium concentration from 3.8 to 5.7 mEq./L. within 20 hours after operation (Fig. 7-A) and Patient No. 20 from 3.8to 6.6 mEq./L. within a period of 10 hours after operation (Fig. 8). As has been clearly demonstrated, many critically injured soldiers, although they maintain their urinary output at a high level, revealed all stages of subclinical renal insufficiency.^{5, 6} Patients with such a subclinical renal failure, although their glomerular and tubular clearances remain low, selectively excrete potassium (Fig. 9).⁷ Their blood urea or nonprotein nitrogen continues to rise for several days; its curve not paralleling the transient rise in plasma potassium depicted in this study (Fig. 10). Patient No. 8 (Fig. 6), although his urinary output remained over a liter per day, demonstrated a more prolonged elevation in potassium concentration, a curve more suggestive of renal insufficiency.

The bank blood used in Korea ranged from 14 to 21 days old. The plasma potassium concentration of this blood was elevated (Table 3) at the time of infusion. Occasionally patients in profound circulatory collapse demonstrated a marked elevation in their plasma potassium concentration as blood was pumped in through several portals, but this was not demonstrated in this survey.

The elevations in the current study were found following the completion of operation and during the period when the plasma hemoglobin was being cleared from the circulation.⁸ One patient who received only dextran and fresh type-specific blood (1 to 5 hours old) demonstrated a similar rise in potassium concentration (Fig. 11).¹

The infusion of potassium in the plasma of stored blood is therefore not the explanation for the increments in plasma potassium demon-

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FIGURE7.
A. During the first few hours after injury, as post-traumatic renal insufficiency
developed, the plasma potassium and sodium concentrations revealed marked inverse changes.
B and C. Demonstrating the transient rise in potassium concentration in the absence of detectable renal failure.

FIGURE8.
During the first few hours after operation, the plasma potassium
concentration increased almost 100 per cent.

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FIGURE9.
The patient with bilateral traumatic amputations of the legs, requiring massive transfusion, developed a subclinical
degree of renal insufficiency yet selectively excreted potassium and retained sodium, as indicated by the sharp
fall in urinary Na/K ratio. His urinary output was never less than 1,000 ml. per 24 hours and his
urinary potassium concentration was maintained at 100 to 125 mEq./L.

FIGURE10.
In spite of the potassium diuresis depicted in Figure 9, the patient developed
a transient rise in his plasma potassium concentration. This elevation, however,
did not parallel the rising B. U. N. concentration.

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FIGURE11.
This patient with a traumatic amputation of a foot and multiple soft tissue wounds was resuscitated with dextran, 2,500 cc., and fresh type-specific blood (1 to 5 hours old), 1,500cc. Nevertheless, the plasma potassium concentration rose over 50 per cent, indicating that the bank blood, routinely used, was not necessarily the cause of the rising potassium concentration.

strated in these casualties. A secondary, in vivo breakdown of red blood cells, with the release of potassium may contribute to the elevation but a more tenable hypothesis is that the increment represents the release of intracellular potassium from the wounded tissues or from cells with altered permeability throughout the body.

Summary

A survey of the plasma sodium and potassium concentrations of 25 severely injured soldiers has been made, including intervals from admission to 10 days postoperative. The potassium concentration of the oliguric patient rises quite rapidly; the non-oliguric patient often demonstrating a transient and less marked elevation. The plasma sodium concentration falls following operation, reaching its lowest level about the third day. Plasma magnesium levels, studied on eight patients, revealed no definite pattern.

References

1. Howard, J. M., Olney, J. M., Frawley, J. P., Peterson, R. E., and Guerra, S.: Adrenal Function in the Combat Casualty. Surgery.(In press.)

2. Strawitz, J. G., Howard, J. M., and Artz, C. P.: Clinical Observations of the Effect of Intravenous Calcium Gluconate on Post-transfusion Hypotension. Final Report to the Army Medical Service Graduate School, Washington, D. C. (August), 1954.

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3. Heagy, F. C.: The Use of Polyvinyl Alcohol in the Colorimetric Determination of Magnesium in Plasma or Serum by Means of Titan Yellow. Can. J. Research 26 E: 295-298, 1948.

4. Frawley, J. P., Howard, J. M., and Artz, C. P.: Changes in Plasma Proteins Following Injury. Report to the Army Medical Service Graduate School, Washington, D. C. (August), 1954.

5. Ladd, M.: Renal Sequelae of War Wounds in Man. Functional Patterns of Shock and Convalescence. Final Report to the Army Medical Service Graduate School, Washington, D. C. (August), 1954. (Chap. 11 in Vol. IV of this series.)

6. Howard, J. M.: Experiences with Shock in the Korean Theater. Shock and Circulatory Homeostasis. Transactions of the 3rd Conference(September), 1953, The Josiah Macy, Jr. Foundation, New York.

7. Howard, J. M.: Preliminary Reports to the Army Medical Service Graduate School, Washington, D. C.

8. 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. (Chap. 6 in Vol. II of this series.)