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Chapter VII

Contents

CHAPTER VII

Effect of Alkalis in Treatment of Traumatic Shock

The use of alkalis has been recommended by some as an adjunct in the treatment of the severely wounded for two reasons. First, it was proposed as a means of combatting the acidosis known to exist in shock; second, it was suggested that production of an alkaline urine might make more soluble any blood or muscle pigments or sulfonamide crystals in the urine. Evidence will be presented here that with judicious use of alkalis it is possible to relieve metabolic acidosis, but that in the presence of shock and the accompanying decrease in renal function, it may be very difficult and even dangerous to attempt to produce an alkaline urine.

Any patient who receives whole blood or blood substitutes of necessity also gets sodium citrate which is employed as an anticoagulant when the blood is collected from the donor. Although the quantity varies slightly, we have assumed that each unit* of blood or plasma contained 2 Gm. of U.S.P. sodium citrate. The quantity of alkali received by a patient transfused with several liters of blood or plasma was therefore considerable. In the patients we observed, any additional alkali given was usually in the form of a 2-percent solution of sodium bicarbonate. This was prepared by adding sodium bicarbonate to distilled water shortly after the water was removed from the autoclave. Although some sodium carbonate undoubtedly resulted from this procedure, no untoward reactions were encountered in a large series of patients to whom this solution was given intravenously. Sodium citrate, 4 or 2.5 percent, in sterile ampules, was also employed in a few instances. The sodium administered in excess of that given as sodium chloride was calculated from the quantity present in sodium citrate or sodium bicarbonate. This figure furnished a convenient index of the total alkali

    *1 unit of blood = 500 cc.; 1 unit of plasma = 300 cc. total volume.


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received, since both sodium citrate and sodium bicarbonate were frequently administered.

In Table 80 the effect of increasing quantities of alkali in relation to the degree of initial shock is shown. Those patients who received between 1 and 5 Gm. of sodium (approximately from 5 to 20 Gm. of sodium bicarbonate or sodium citrate) still had an acid urine after 20 to 30 hours, and they showed no remarkable rise in plasma carbon-dioxide combining power. In those who received between 5.1 and 10 Gm. of sodium the urine became alkaline only if they had had little or no initial shock. There was a significant change in preoperative and postoperative plasma carbon-dioxide combining power only in those who had had moderate or severe shock, but their urines remained acid.

Inspection of the data on individual patients (Table 80) who received between 10.1 and 20 Gm. of sodium shows that of six who had been in moderate or severe shock, only one was producing an alkaline urine 24 hours later and the remaining five still had acid urines 26 to 34 hours after wounding. The two patients with no shock and slight initial shock respectively both had highly alkaline urines. The plasma carbon-dioxide combining power rose significantly in five of seven patients on whom postoperative determinations were made.

These observations show rather clearly that in patients who have had severe or moderate shock, an alkaline urine is not usually produced even after administration of large quantities of alkali, although the metabolic acidosis may be relieved. The dangers of producing severe alkalosis in such patients, and a partial explanation of their inability to form an alkaline urine become apparent in Tables 81, 82, and 83, and Chart 28 which show the sequence of events in three patients with moderate or severe initial shock who received large quantities of alkali. The cases are summarized as follows:

Cases of Alkalosis

Case 108 (Table 81).-This patient, who had severe shock on hospital entry, received 34 Gm. of sodium bicarbonate and 24 Gm. of sodium citrate within the first 24 hours after admission. The plasma carbon-dioxide combining power responded to this excess alkali by rapidly rising to 34 milliequivalents per liter, but despite this relative alkalosis the urine did not become alkaline until the third postoperative day. The plasma chloride level fell although scarcely any chloride was excreted in the urine. Coincident with these changes in acid-base metabolism, the output of urine was very small, the specific gravity of the urine fell, the plasma nonprotein level rose, and the urea nitrogen excretion was minimal. The patient died in uremia on the third postoperative day.


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TABLE 80.-RELATIONSHIP OF SODIUM INTAKE AND DEGREE OF INITIAL SHOCK TO PLASMA CARBON-DIOXIDE COMBINING POWER AND pH OF URINE


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TABLE 81.-CHANGES IN ACID-BASE METABOLISM AND COINCIDENT FINDINGS IN A PATIENT WHO
RECEIVED EXCESS ALKALI
Severe Initial Shock and Subsequent Death from Posttraumatic Renal Insufficiency
Case 108

Case 112 (Table 82).-Twenty Gm. of sodium bicarbonate and 16 Gm. of sodium citrate were administered within 6 hours after this patient entered the hospital in severe shock. The pH of the venous blood and the plasma carbon-dioxide combining power promptly rose to levels indicative of moderate alkalosis, but the urine did not become alkaline until nearly 24 hours after the alkali had been administered. Although urinary output was normal after the first day, the plasma nonprotein nitrogen level had risen to 67 mg. per 100 cc. by the second postoperative day, when the patient was evacuated. Plasma chloride levels fell and chloride excretion was low. Subsequent follow-up revealed that nitrogen retention persisted for 6 days; the status of the acid-base metabolism could not be followed.

Case 107 (Table 83 and Chart 28).-This patient, admitted in moderate shock, received 35 Gm. of sodium bicarbonate and 28 Gm. of sodium citrate on the day of operation, and 15 additional grams of sodium bicarbonate early on the first postoperative day. The resulting severe and prolonged alkalosis is evident in the high plasma carbon-dioxide combining


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TABLE 82.-CHANGES IN ACID-BASE METABOLISM AND COINCIDENT FINDINGS IN A PATIENT
WHO RECEIVED EXCESS ALKALI
Severe Initial Shock, Subsequent Nitrogen Retention, and Recovery
Case 112

 TABLE 83.-CHANGES IN ACID-BASE METABOLISM AND COINCIDENT FINDINGS IN A PATIENT
WHO RECEIVED EXCESS ALKALI
Postoperative Alkalosis and Azotemia, Resulting in Death
Case 107

power and blood pH. Considerable ammonium chloride was given on the fourth and fifth postoperative days in an unsuccessful attempt to relieve the alkalosis. In this case also there was a marked lag in the production of an alkaline urine after metabolic alkalosis appeared. By the fourth postoperative day, although severe alkalosis persisted, the patient was no longer able to excrete an alkaline urine. Plasma chlorides fell to phenomenally low levels


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CHART 28.-EFFECT OF ALKALI ADMINISTRATION IN FATAL CASE (CASE 107)

in this patient (56 milliequivalents per liter the day before death); urinary chloride excretion was practically nil throughout his course. The plasma nonprotein nitrogen level rose,


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and the patient died on the sixth postoperative day, with renal failure in our opinion an important contributory factor in his death.

The low plasma chloride levels in these three cases are partly explained by the reciprocal relationship of carbon dioxide and chloride in the plasma. That this is not the entire explanation is evident in the fact that in two (Cases 107 and 108, Tables 81 and 83) the plasma chloride level continued to fall after the plasma carbon-dioxide combining power had also begun to decline. Hence it would appear that the mechanisms producing hypochloremia, frequently a feature of lower nephron nephrosis following traumatic shock (see Chapter V), were also operative in these cases.

SUMMARY AND CONCLUSIONS

Reasons that have been advanced for using alkalis in traumatic shock are (1) to relieve metabolic acidosis and (2) to produce an alkaline urine. We found that large quantities of alkali are necessary to relieve acidosis when it is severe; that is, in patients in shock. If in addition enough extra base is given to produce an alkaline urine in these patients, the margin of safety between normal acid-base equilibrium and uncompensated alkalosis may be very small. In the event that alkalosis does result, it may materially contribute to renal failure. Three cases in which this may have occurred have been presented.

The mechanism of the low alkali tolerance in these patients is not clear. The impaired ability of the kidneys to excrete excessive amounts of sodium apparently is associated with the general impairment of renal function that occurs in all patients suffering from shock, and continues for some time after the shock has been relieved, as was brought out in Chapter III.

Because the evidence is so meager that an alkaline urine will prevent renal complications in the type of patient studied here, and because of the dangers inherent in trying to produce such a urine, the use of alkalis for this purpose is not recommended. Small quantities of alkali sufficient to relieve metabolic acidosis, if judiciously employed, probably are advisable. The amount routinely given with citrated whole blood or blood substitutes will in most instances be adequate for this purpose.

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