CHAPTER VII
Effect of Alkalis in Treatment of Traumatic Shock
The use of alkalis has been recommended by some as an adjunct in thetreatment of the severely wounded for two reasons. First, it was proposedas a means of combatting the acidosis known to exist in shock; second,it was suggested that production of an alkaline urine might make more solubleany blood or muscle pigments or sulfonamide crystals in the urine. Evidencewill be presented here that with judicious use of alkalis it is possibleto relieve metabolic acidosis, but that in the presence of shock and theaccompanying decrease in renal function, it may be very difficult and evendangerous to attempt to produce an alkaline urine.
Any patient who receives whole blood or blood substitutes of necessityalso gets sodium citrate which is employed as an anticoagulant when theblood 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 transfusedwith several liters of blood or plasma was therefore considerable. In thepatients we observed, any additional alkali given was usually in the formof a 2-percent solution of sodium bicarbonate. This was prepared by addingsodium bicarbonate to distilled water shortly after the water was removedfrom the autoclave. Although some sodium carbonate undoubtedly resultedfrom this procedure, no untoward reactions were encountered in a largeseries of patients to whom this solution was given intravenously. Sodiumcitrate, 4 or 2.5 percent, in sterile ampules, was also employed in a fewinstances. The sodium administered in excess of that given as sodium chloridewas 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 frequentlyadministered.
In Table 80 the effect of increasing quantities of alkali in relationto the degree of initial shock is shown. Those patients who received between1 and 5 Gm. of sodium (approximately from 5 to 20 Gm. of sodium bicarbonateor sodium citrate) still had an acid urine after 20 to 30 hours, and theyshowed no remarkable rise in plasma carbon-dioxide combining power. Inthose who received between 5.1 and 10 Gm. of sodium the urine became alkalineonly if they had had little or no initial shock. There was a significantchange in preoperative and postoperative plasma carbon-dioxide combiningpower only in those who had had moderate or severe shock, but their urinesremained acid.
Inspection of the data on individual patients (Table 80) who receivedbetween 10.1 and 20 Gm. of sodium shows that of six who had been in moderateor severe shock, only one was producing an alkaline urine 24 hours laterand the remaining five still had acid urines 26 to 34 hours after wounding.The two patients with no shock and slight initial shock respectively bothhad highly alkaline urines. The plasma carbon-dioxide combining power rosesignificantly in five of seven patients on whom postoperative determinationswere made.
These observations show rather clearly that in patients who have hadsevere or moderate shock, an alkaline urine is not usually produced evenafter administration of large quantities of alkali, although the metabolicacidosis may be relieved. The dangers of producing severe alkalosis insuch patients, and a partial explanation of their inability to form analkaline urine become apparent in Tables 81, 82, and 83, and Chart 28 whichshow the sequence of events in three patients with moderate or severe initialshock who received large quantities of alkali. The cases are summarizedas follows:
Cases of Alkalosis
Case 108 (Table 81).-This patient, who had severeshock on hospital entry, received 34 Gm. of sodium bicarbonate and 24 Gm.of sodium citrate within the first 24 hours after admission. The plasmacarbon-dioxide combining power responded to this excess alkali by rapidlyrising to 34 milliequivalents per liter, but despite this relative alkalosisthe urine did not become alkaline until the third postoperative day. Theplasma chloride level fell although scarcely any chloride was excretedin the urine. Coincident with these changes in acid-base metabolism, theoutput 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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Case 112 (Table 82).-Twenty Gm. of sodium bicarbonateand 16 Gm. of sodium citrate were administered within 6 hours after thispatient entered the hospital in severe shock. The pH of the venous bloodand the plasma carbon-dioxide combining power promptly rose to levels indicativeof moderate alkalosis, but the urine did not become alkaline until nearly24 hours after the alkali had been administered. Although urinary outputwas normal after the first day, the plasma nonprotein nitrogen level hadrisen to 67 mg. per 100 cc. by the second postoperative day, when the patientwas 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).-Thispatient, admitted in moderate shock, received 35 Gm. of sodium bicarbonateand 28 Gm. of sodium citrate on the day of operation, and 15 additionalgrams of sodium bicarbonate early on the first postoperative day. The resultingsevere and prolonged alkalosis is evident in the high plasma carbon-dioxidecombining
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TABLE 82.-CHANGES IN ACID-BASEMETABOLISM AND COINCIDENT FINDINGSIN A PATIENT
WHO RECEIVED EXCESSALKALI
Severe Initial Shock, Subsequent Nitrogen Retention,and Recovery
Case 112
TABLE 83.-CHANGES IN ACID-BASEMETABOLISM AND COINCIDENT FINDINGSIN A PATIENT
WHO RECEIVED EXCESSALKALI
Postoperative Alkalosis and Azotemia, Resulting in Death
Case 107
power and blood pH. Considerable ammonium chloride wasgiven on the fourth and fifth postoperative days in an unsuccessful attemptto relieve the alkalosis. In this case also there was a marked lag in theproduction of an alkaline urine after metabolic alkalosis appeared. Bythe fourth postoperative day, although severe alkalosis persisted, thepatient was no longer able to excrete an alkaline urine. Plasma chloridesfell to phenomenally low levels
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CHART 28.-EFFECTOF ALKALI ADMINISTRATION INFATAL CASE (CASE107)
in this patient (56 milliequivalents per liter the daybefore death); urinary chloride excretion was practically nil throughouthis course. The plasma nonprotein nitrogen level rose,
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and the patient died on the sixth postoperative day, withrenal failure in our opinion an important contributory factor in his death.
The low plasma chloride levels in these three cases are partly explainedby the reciprocal relationship of carbon dioxide and chloride in the plasma.That this is not the entire explanation is evident in the fact that intwo (Cases 107 and 108, Tables 81 and 83) the plasma chloride level continuedto fall after the plasma carbon-dioxide combining power had also begunto 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 shockare (1) to relieve metabolic acidosis and (2) to produce an alkaline urine.We found that large quantities of alkali are necessary to relieve acidosiswhen it is severe; that is, in patients in shock. If in addition enoughextra base is given to produce an alkaline urine in these patients, themargin of safety between normal acid-base equilibrium and uncompensatedalkalosis may be very small. In the event that alkalosis does result, itmay materially contribute to renal failure. Three cases in which this mayhave 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 sodiumapparently is associated with the general impairment of renal functionthat occurs in all patients suffering from shock, and continues for sometime after the shock has been relieved, as was brought out in Chapter III.
Because the evidence is so meager that an alkaline urine will preventrenal complications in the type of patient studied here, and because ofthe dangers inherent in trying to produce such a urine, the use of alkalisfor this purpose is not recommended. Small quantities of alkali sufficientto relieve metabolic acidosis, if judiciously employed, probably are advisable.The amount routinely given with citrated whole blood or blood substituteswill in most instances be adequate for this purpose.
