Studies on Fluid and Electrolyte Alterations During Transurethral Prostatectomy: II

THE JOURNAL OF UROLOGY

Vol. 86, No. 4 October 1961 Copyright © 1961 by The Williams & Wilkins Co.

Printed in U.S.A.

STUDIES ON FLUID AND ELECTROLYTE ALTERATIONS DURING TRANSURETHRAL PROSTATECTOMY: II CAPT. FRANKE. CECCARELLI (MC) AND CAPT. PERRY C. SMITH (MC) From the Urological Service, Department of Surgery, and the Radioisotope Clinic, Radiology Service, Brooke General Hospital, Fort Sam Houston, Texas

The transurethral resection (TUR) reaction syndrome, occurring after transurethral prostatectomy, has been described by many authors and consists of hypertension, bradycardia, restlessness, apprehension and blurring of vision with ultimate convulsion, coma, vascular collapse, anuria and death. 1- 4 Occasionally the syndrome may present initially with hypotension or normotension instead of hypertension. 5 • 6 Intravascular absorption of irrigating solution during transurethral prostatectomy has been proven by many methods. 3 • 7-u Hemolysis of red Accepted for publication March 1, 1961. Read at annual meeting of South Central Section of American Urological Association, Inc., Albuquerque, N. M., September 25-28, 1960. 1 Creevy, C. D. and Webb, E. A.: Fatal hemolytic reaction following transurethral resection: A discussion of its prevention and treatment. Surg., 21: 56-66, 1947. 2 Griffin, M.: Toxic symptoms accompanied by hemolysis during transurethral prostatectomy. J. Urol., 59: 431-436, 1948. 3 Hagstrom, R. S.: Studies on fluid absorption during transurethral prostatic resection. J. Urol.,

cells secondary to pickup of distilled water is not necessary for the syndrome to occur. 3- 5 A postoperative decrease in serum sodium concentration occurs after transurethral prostatectomy and is associated with the TUR syndrome; 3 • 4 • 7 however, there is no consistent relationship between the magnitude of this decrease and the occurrence or severity of the syndrome. 5 In the previous study, 5 it was demonstrated that during TUR there is a decrease in the circulating plasma volume and in the serum sodium concentration, and an increase in total body weight and in the peripheral venous hematocrit. Acute dilutional hyponatremia caused by increase in total body water (as manifested by the gain in weight) was shown to be inadequate to explain the extent of decrease in serum sodium concentration; consequently an absolute loss of sodium from the body during TUR was postulated. This study was undertaken to prove or disprove that postulation.

73: 852-859, 1955. 4 Harrison, R. H., Boren, J. S. and Robinson, J. R.: Dilutional hyponatremic shock; another concept of the transurethral prostatic resection reaction. J. Urol., 76: 95-110, 1956. 6 Ceccarelli, F. E. and Mantell, L. K.: Studies on fluid and electrolyte alterations during transurethral prostatectomy: I. J. Urol., 86: 75-82

1961. 6 Marx, G. and associates: Intravenous infusions of 10 per cent cytal, 5 per cent dextrose/ water or plavolex in dogs. J. Urol., 84: 424-427,

1960. 7 Maluf, N. S. R., Boren, J. S. and Brandes, G. E.: Absorption of irrigation solution and associated changes upon transurethral electrorcsection of prostate. J. Urol., 76: 824-836, 1956. 8 Creevy, C. D.: Hemolytic reactions during transurethral prostatic resection. J. Urol., 68:

125-131, 1947. 9 Landsteiner, E. K. and Finch, C. A.: Hemoglobinemia accompanying transurethral resection of the prostate. New Eng. J. Med., 237: 310-312,

1947.

10 Griffin, M., Dobson, L. and Weaver, J. 0.: Volume of irrigating fluid transfer during transurethral prostatectomy, studies with isotopes. J. Urol., 74: 646-651, 1955. 11 Taylor, R. 0. and associates: Volumetric, gravimetric and radioisotopic determination of fluid transfer in transurethral prostatectomy. J. Urol., 79: 490-499, 1958.

434

METHODS AND MATERIAL

Eight patients undergoing transurethral surgery for obstructing prostatism on the urological service at Brooke General Hospital were studied. Selection was based solely on the need for prostatectomy. Final pathological diagnosis of benign prostatic hypertrophy was found in all patients. All resections were done by urological residents. All patients had spinal anesthesia. The Stern-McCarthy 28F resectoscope was used exclusively. The Liebel-Flarshiem Bovie electrosurgical unit was used; in general the slightly damped spark-gap current set at 45 was used for cutting; coagulation was accomplished with the spark-gap current set at 55. The irrigating solution was 1.5 per cent glycine* at a height of 50 cm. The amount of tissue resected varied between 5 and 50 gm., with a mean of 22 gm. The operating time varied between 20 and 95 minutes,

* Glycine: Prepared in Brooke General Hospital pharmacy from commercial preparation by Baxter Laboratory.

FL[JID A:'\TD ELECTROLYTE ALTERATIONS DURING TRANSURETHRAL RESECTION

with a mean of 52 minutes. Removal of all aclenom.atous tissue was atkmpted in all cases. One patient (Ko. 1) rnrniting surgery was stucli('.d; values obtained from this man were used as controls. One patient (:'.\To. 2), a 22-ycarold man "-ho undenvent a varicocelectomy, was also 8tuclicd as a control. Each patient was injPctecl with a measured dose of radioactive sodium (:\ a12), obtained from i\.bbott Laboratories; the dosages varied between 25.6 mir:rocuriPs and 29.6 microcnries with a mean of 27. 7 microC'uries. Daily pre- and postoperative blood sarnp1es were obtained at 8 a.m. ,md thP total daily urinP output was saved. During surgery blood samples were obtained approximatrly every 15 minutes. Two or three blood samples were obtained in the 3 hour period following surgery. All irrigating solution used was recovered and measured every 15 minutes during surgery; aftPr thorough mixing, 1500 cc aliquots ,vere saved. All postoperative irrigations 11ml catheter drainage were treated in the same manner. All specimens, plasma, urine and irrigating fluids ,vere analyzed for sodium12 by the Laboratory Service, Brooke General Hospital. Blood samples wen) analyzed in the radioisotope clinic, Brooke General Hospital for N a 22 a;,; follows: 5 cc plasma was counted in a welltype scintillation ('OUukr and compared to a standard. This standard was prPpared by diluting to 500 cc an amount of Na 22 exactly equal to that originally given to each patient. From this dilution, l cc was taken, diluted to 5 C(' and counted in the same well-typc counter. Specimens were {'Ountcd for a minimum of 104 counts, insuring an ,wcuracy of I per cent or hctter. Urine samp!Ps \Yerc analyzed for :'.\Ta22 as follows: :i 5 cc aliquot of the 24 hour urinary -collection was countccl in a well-type scintillation {'Ounter and comparPd with the same standard as the blood. Irrigating solutions were analyzed for N a 22 as follows: representative 1.'500 ce aliquots of the total volume were counted in a modified J\Iarinelli fl.ask and compan!d against a second standard. This standard \\'as prepared by taking 2 cc of the initial blood ~tandard and clilutiug it to 1500 cc. 12 Methods for sodiwn (le terminations in Brooke General Hospital Laboratory Service: A rapid method for determination of sodiL1m and potassium in human blood serum or plasma. Coleman fostruments lVIanual T-Jil,2. Maywood, Ill., 1956.

Specimens were counted to a m1mmurn of J counts. Exehangeable sodium and time of hio logical equilibrium were calculated DB describ,·.d by Adesman. 13 Sodium lost in irrigating solution was caln1 lated as the per cent loss of Narc: on the morn· ing of surgery. The formula nsed n-as:

where ::'1faL = sodium lost in irrigating 1 = irrigating solution r:ounts; S1. = solution standard counts; Na1 = 1:ounts (standard); Na, = cumulative urinary counts 011 the morning of surgery and N iiE body sodium. Fecal and svreat 1os8es~ rninin1al, were ignored. 14 The prPsence or absence of hemolysis in Pa('!, case was determined by observation of tlw 8(·ru1n in a postoperative specimen of venous blood taped to the foot of the patient's bed and allow('(! to dot. Because of a change in the was impossible to obtain accurate pre- and postopcrati ve \\-eights, as was done in the first serier,: studied. The results of these studies arc tabulated table 1. Statistical evaluation of all data was madi: using the "t" test with sig-nificance at 5 per or less. 15 Using the criteria previously patient in this series had either a mild or scn°re TUR syndrome. Two patients (Nos. 4 and 5) h;1d an elevation of blood pressure of SO or more mll\. Hg. with no other operative or postopernti\-e or symptoms. One patient had an anesthetic level above T-2 with resultant tory distress but no other signs or symptoms. Hemolysis of red cPlls wa::; not observed. in ;1nv of these patients. u Adesman, J. a.nd associates· Simult.a.neom, measurement of body sodium and poLassinm usi uv Na 22 and K12. Meti,b., 9: 561-560, 1060. Veall, N. and associates: An improv;;d method for clinical studies of 1.oi.al excha.ngea.blr: sodium Lancet, 1; 4Hl-422, Hl55. 15 Batson, H. C.: An Introduction t.o Sta1istics in the .Medical 1-,ciences. Minneapolis. ;\linn. Burgess Pnbli.~hing Co., HJ56, pp. IG-21.

436

CECCARELLI AND SMITH TABLE

1.

Results of studies performed Pre & Postop Values ReWt sect Tissue Irrig. Age (Lbs) Pt. BGH Sol. Time Resect No. (L) (min.) (gm.)

-

---

Ave. Na Loss Fluids in OR* Preep (mer day

Na (meq/L) Pre

Post

Na22 (Cts X 10 6)

Pre

Post

NaE (m.Eq) Pre

Post

Na loss loss Na loss during surg Na 18 hrs 1st (m.Eq) after postop day surg (mEq) (mEq) Na22

Na2a

-- - - - - ------ ------ ---- - - - -

-- -- --

1.

5632 039

73

173

(control)

2.

5596 006

22

157

(varicocele-control)

500 5%

151

141

139

. 711

3368

3418

20

23

3.

5538 051

66

180

65

35

30

100 5%

165

138

135 I. 185 1.146

3139

3007

45

58

26

ND

4.

5545 054

70

158

40

10

18

225 5%

149

141

137 1.02

.956

3234

3411

32

47

40

ND

5.

5599 007

61

160

95

17

23

150 bl 350 5%

183

146

134 1.165 1.05

3394

3470

58

ND

139

ND

6.

5546 081

70

183

60

40

25

50 bl 200 5%

290

137

133 1.018

.901

3282

3175

79

75

110

67

7.

5598 011

59

200

15

5

6

100 5%

61

138

137

.951

.925

3411

3728

24

6t

39

23

8.

5586 026

71

221

50

28

19

100 5%

200

141

138

.639

.624

4893

4936

98

ND

230

92

9.

5621 013

62

150

20

5

10

100 5%

272

140

142

.676

.634

3290

3320

13

ND

153

150

10.

5660 019

73

170

70

33

22

300 bl 500 5%

182

141

138 1.474 1.388

4060

ND

159

229

ND

ND

I

207

I

.725

145

•bl= whole blood; 5% = 5% glucose/water; ND = Not done. Inaccurate at this concentration (12).

t

In all patients, biological equilibrium of Na22 was achieved before surgery and in the majority before the sixth day after injection. In this series, there was a significant decrease in postoperative serum sodium averaging 3.4 meq/L ± 1.21 meq/L. No significant statistical difference was present between the serum sodium decreases in this series and those in the entire previous series. No significant statistical difference was present between the serum sodium decreases in this series and that of those patients in the previous series who had a reaction. Measured by Na22 there was a statistically significant loss of sodium during the operative and immediate postoperative period, averaging 58.6 mEq ± 15.7 mEq. Measured by flame photometer, the loss averaged 73 mEq ± 33.4 mEq. There was no statistical difference between these figures. There was a significantly greater loss of sodium during the operative period than in a like pre-

operative period; the average increase in sodium loss being 38 mEq ± 12.5 mEq. In the first 18 hours after surgery, the average sodium loss was 105 mEq ± 25.3 mEq. This was not significantly greater than in a like preoperative period. In the following 24 hours, there was a significant decrease in urinary loss of sodium compared to the daily preoperative level. This loss averaged 63.5 mEq ± 37.8 mEq. The amount of sodium loss could not be correlated to the weight of prostatic tissue removed or the amount of irrigating solution used. In general, the longer the resection the greater the amount of sodium loss; this correlation was not statistically significant. Comparing the values obtained when surgery was started to those at the completion of surgery, serum concentration of Na22 decreased in 100 per cent of patients, total serum sodium (N a2 H 22 ) decreased in 88 per cent of patients; the specific

.FLUID AND ELECTROLYTID ALTERATIONS DURING 'I'RANS.CRETHRAL RESl~C'l'lOK

activity of the scrum decreased in 88 per cc:nt of patients. Of the patients who had no exogenous sodium (infusion or transfusion), serum concentration of Na 22 decrcrrncd in HlO per cent of patients, total serum sodium cleereased in 83 per cent of patients, ancl the ,;pccific. activity decreased in 83 per cent of patients. On the morning of smgny, N aE averaged 3567 T,venty-four homs after surgery, in those patients who had no exogenous sodium, Narn apparently increased in 80 per cent with an average increase of 66 DISCUSSI01'

These resections wc,rc clone by different residents ut different of training; consequently it 1n1s not surprising to find a lack of correlation between the amount of ti~stw removed, the amo1rnt of irrigating sollltion used and the time of resection. These factor,; were evident in the first report. From the experimental standpoint alone, it is regrettable that a T(;R syndrorne did not develop in any patients in this series. vYhile it could be nrgurd that entirely different values might be found in patients with the TUR syndrome, there arc no significant statistical differences in the changes in the (fata obtained to date between pa.tients whose coursr-' 1nts benign and those whm,e course was not. In addition there are no statistical differences in any measured values between this serir's and the firnt one reported; ccmsequcntly they may he compared analytically. The purpose of this series of studies is to analyze the over-all changes in patients undergoing TUR n1ther than specifically those: whose course is not benign; consequently, inferences clrawn as to the loBs of sodium should be rclati,-ely correct. Evaluation of the data obtained reveals the following interesting findings: 1) As was expected, an over-all decrease in serum sodium com·entration occurred during 'l'UR 2) As had been previously postulated, a loss of sodium was found in the irrigating solution during surgery, mr11surrd hy both flame photom .. eter and radioisotope methods. This is gn'ater than that expected from 11rine alone and is from the prostatic fossa, 3) There was :rn apparent increase in N aE after surgery. 4) There was a significant decrease in the

specific activity of the serum rn postoperative period. Calculations were rwrformccl on tlw tive serum sodium levels expected frorn changes and from dilution and ]os~ in solution; these calculations wc'n: corrected for exogenous sodium ndn1iuistC'recl (table following is apparent: 1) The actual postoperatin: serum ~odiu1n concentration was higher than that from the NaP serum concentratiou

of 2.8 2) The actual SCl'U.Hl HO(hurn conc.;entration in.is higher ttuw that from the cornhinatiou of loss in irrigating wlutH,11 and extracellular dilution an av('tI1gc ul

Since all exogenous sodium administered 1YaS accounted for in these data and calculations, jt mrnlcl appear there is an enclogrnous infusion ot nonrqnilibrnted sodium into tlw extraccllul:Lt 2.,~ spar,e amounting to Previous workers ill the field of sodium metaholisrn have shown that 4!5 per cent of sc;(linru is found in bone and only 7-10 JWr C('nt of tot,u l body sodium is intracellnlar_ 30-40 per ct-·ut of bone sodium is exchangeable with radin-sodi1m1 in 24 hours; after that period of tberc' very slow curn: with equilibrium about per cent of total bone: ~odium. 1-uc- 12 handled by the body iu the sanw way aii ;,;tab],, sodiumrn Scrum osmolarity i'ondates closdy with senmJ sodium concentration; h01wver serum mdin 111 conc:entration is poorly correlated with '\'a E _2l1 Nichols and Xichol8 21 dcmonstrakd tlint acute sodium loss, bone contributed (l\'l'r 2:.i cent of the sodium Jost and body cells ouJ~· ii 1wr cent; the remainder is from tht: r,xt.racdluhiJ· 11i Nichols, G., ,Jr. and bone in sodium metabolism.

Hole 5: IJ/:',-/4(\

1956, 17 Bergstrom, W. II. in total body sodium

of hont: Cli11 !n

vestig., 34: \)97-1004, 1\i55. 18 Bergstrom, vY. H .. Thu skeleton as an PlPclrn .. lyte reservoir. 1\fob1b., 5: 1Df>l\. 10 Martin, M. M. and Walker, . : StlHlies w, :Kr1 22 : An assessment. of sodimn balance ami rfo,

tril.rntiou. 20 Edelman. l.

6: 4G6478, Hl::i7 : Interrnlations between

sodium concentratimrn, .,erum osmolariiv :rnd tot,d exchangeable sodimn, t.01,al exclrniigcalih potassium and total bodv ,Yater . .J C\in. Inve,,;1.i,:r 37: 12:3G-125G, 1\i58. .. .. . . 21 Nichols, G., Jr. and :,ichols, ?\ _: tissue composition during ac1tte sodium Am. J. l'hy;;iol., 186: :)8:3-3D2, UJ56.

438

CECCARELLI AND SMITH TABLE

2

A. Expected serum level based on counts of Na22 Pt.

2. 3. 4. 5. 6. 7. 8. 9. 10.

Actual postop Na (meq/L)

139 135 137 134 133 137 138 142 138

Expected Na (pre-op Na-% Ct drop) (meq/L)

(141 (138 (141 (145 (137 (138 (141 (140 (141

- 2.3) = 138.3 - 4.4) = 133.6 - 6 ) = 135 - 14.3) = 130.7 - 6.4) = 130.6 - 3.9) = 134.1 - 3.2) = 137.8 - 8. 7) = 141.3 .8) = 140.2

Total gain (meq/L)

Exogenous gain (meq/L)

.7 1.4 2 3.3 3.6 2.9 .2 10.7 -2.2

1. 7 .7

5.7

Net Serum gain (meq/L)

.7 1.4 2 1.6 2.9 2.9 .2 10.8 3.5

Mean Net Serum Gain of Endogenous Na-2.8 meq/L B. Expected serum sodium levels from dilution and irrigating solution loss (mean values) Preop weight-75 kg. Preop extracellular H20-75 X 20%-15 L Preop serum Na-140.4 mEq Postop serum Na-137 Drop from irrigating loss Loss from dilution Loss-58.7 mEq Gain in wt 5 Expected decrease-loss/extracell. H20Postop extracell. H20-½ gain + preop extracell. 3.8 meq/L H20-15.27 L Total preop Na-140.4 X 15 = 2107 mEq Expected postop level 2107 /15.27-137.9 Drop by dilution-140.4 - 137 .9-2.5 meq/L Total expected decrease-2.5 + 3.8 = 6.3 meq/L Expected Na level-140.4 - 6.3 = 134.1 meq/L Total gain of endogenous Na-137 - 134.1 meq/L = 2.9 meq/L Gain of exogenous Na*-.9 meq/L Net gain of endogenous Na-2.9 - .9 = 2 meq/L * See A space. A fall of 7 meq/L serum sodium gave a clinical picture of hyperpnea, hypotension, vascular collapse and shock in dogs; 25 per cent of these experimental animals died, while the remainder were lethargic and prostrate for two or three days. Relative intracellular hyperosmoJarity was shown in these animals. Bergstrom22 on an experimental basis showed that in sudden base loss bone may contribute the equivalent of 33 mEq sodium in a 70 kg. man. In the presence of acute depletion, 28 per cent of bone sodium is rapidly mobilized; exchangeable sodium (N aE) may be entirely removed by peri22 Bergstrom, W. H.: Bone as a sodium and potassium reservoir. J. Clin. Investig., 31: 617, 1952.

toneal dialysis while extracellular sodium concentration is unchanged.17 In a healthy individual, there are no dramatic changes in NaE when trauma occurs; however, in the elderly or chronically debilitated individual there is a sudden elevation of N aE after trauma. 23 Using a whole-body counter, Martin and associates24 showed that even when equilibrium has been reached whole body activity decreases immediately after surgery without urinary loss of 23 Moore F. D.. and associates: Total body water and electrolytes: Intravascular and extravascular phase volumes. Metab., 5: 447-467, 1956. 24 Martin M. M. and associates: Sodium balance studied with 22N a and an external counter for measuring whole-body radioactivity. Lancet, 1: 653-656, 1957.

FLUID AND J
sodium, Three to five later it returns to levels, Based on these previous reports, one may intc>rpret the prPsent data to indicate that during trauma (including surgery) or acute sodium depletion, previ011sly nonexchangeable bone Rton's of sodium rapidly become exchangeable and eontribute to extracellular sodium coneentration. This tends to maintain the extracellular osmolarity, minimizing the increase in intracellular water and resultant decrease in intravascular volume." This would appear to be an important honwostatic principle. As has been shown in this study, an acute sodium loss occurs during TUR and there is apparently a. rapid mobilization of sodium much like that in the exp<~rimcntaI animal undergoing sodium depletion, CONCL USJONS

These studies eonclusively demonstrate ,t sodium Joss as well as a fluid pick-up during TUR. The effect of the sodium loss is to decrease the extracellular sodiu rn concentration with a resultant d<'creascd extracellular osmolarity. ·when this happens, water will enter the cells, creating relative cellular edema. The body cornbats this situation an endogenous infusion of sodium from previously inert stores, presumably in bone, thereby maintaining a relatively normal scrum sodium concentration, The effect of the fluid piek-up is also to decrease the extracellular sodiurn concentration, this time dilution; again cellular cdcrna results and sodium is mobilized from bone to maintain equilibrium. On this basis, the following hypothesis of the pathophysiology of transurethrnl prostatectomy is rn· ,rn,.,.,., During_TUR two factors are occurring simultaneously, a loss of body sodium and an increase in body water, both resulting in a dccreasE in extracellular ornrnla.rity. The TUR syndrome occurs when there is either an exrapid infusion of water, an extremely rapid loss of sodium, or a less rapid combination of both, such as to exceed the compensatory scrdiurn supplying mechanism resulting in severe extracellular hypoosrnolarity and derangement of body fluids. :Sirwe a low scrum sodium does not necessarily m('an a TUR syndrome and the syndrome may 00

occasionally ocnir withoL1t nmrked of the serum sodium, other factors may be opera. tiY<:. However, the vast majority of rns<'s of TFR syndrome seem to ocem as a result of thr: afcn'f,-· mentioned situation,,;, PROPHYLAXIS AND 'l'R..l:;A'J.'lVIEKT

The TUR syndrome is a. eompliea.ted shift body fluids and electrolytes akin to watd' intoxication and is caused primarily relative or absolute decrease of extra.cellular sodium, Even when mild symptoms the of patients can adjust to the situation and benign course. Some will not; certain prophylactic rneasm·rs should be routim· for all cases of transurcthral prostat.ectorny. In the event the syndrome develops, imrn,·drnt.e active treatment should be earried out. Preoperatively, any relative decrease in sodium should be corrected, Intra.venous or oral fluids should not be used in tbc 12 hours bdotc· surgery. During surgery an ,,, ___, ,,..,., rninimal amount of intravenous fluid should ht>
440

CECCARELLI AND SMITH

be administered through a three-way stopcock with a venous pressure set attached so that determinations may be made every ten minutes. Improvement is usually rapid, although final resolution of all effects may take 24 hours or longer. The efficacy of this treatment is demonstrated in the following case report, a patient who was not studied with N a22 • CASE REPORT

W. R., BGH No. 5693016, was a healthy, normotensive (140/80) man of 69 years who had a TUR of 16 gm. obstructing prostatic tissue. Resecting time was 80 minutes; it was noted during the procedure that the trigone was undermined and what appeared to be fat droplets were seen in the prostatic fossa indicating capsular perforation; the suprapubic area remained soft. A steady rise in systolic blood pressure of 40 mm. Hg. was noted at the end of the procedure and the patient became slightly nauseated. In the immediate postoperative period, he was slightly lethargic but otherwise normal. Blood pressure continued elevated to 180/100 with a pulse of 70. Twenty-two hours after surgery, the patient vomited and was completely uncooperative. Blood pressure was 190/90 and he was cold and clammy. Twenty-three hours after surgery, a serum sodium level (which was not reported for 5 hours) was 125 mcq/L. Twenty-four hours after surgery, the patient had a typical grand ma! seizure which lasted about five minutes and subsided spontaneously. Blood pressure 5 minutes after this seizure was 280/120. Blood for serum sodium concentration was obtained; this was eventually reported as 119 meq/L. While awaiting this report, hypertonic (5 per cent) saline was immediately started at 40 drops/minute. Over the next 15 minutes, the blood pressure dropped to 190/100; the infusion infiltrated and the blood pressure remained at the level for the 15 minutes it took to restart the saline. Twenty minutes after saline was restarted, the blood pressure stabilized at 148/88; pulse was 90. A total of 200 cc hypertonic saline was administered over 2½ hours. Three hours after discontinuing the saline, blood pressure slowly rose to 190/120. One hundred cubic centimeters more of hypertonic

saline were administered and pressure fell to normotensive levels within 30 minutes. A total of approximately 225 mEq sodium had been administered. During the 6 hours after saline was started, urinary output averaged 180 cc/hr. This urine contained 41 meq/L sodium. Despite therapy the patient remained comatose during most of this second 24 hours after surgery. Medical and neurology consultations were obtained. Pertinent notes of their findings were "T-102, BP 160/90, P-96, R-34; unresponsive, eyes deviated to right, hyperventilating, neck supple; no nystagmus or papilledema. Crepitant rales over both lung fields. Bilateral Babinski, increased DTR's on right, less resistance to passive movement on right arm and leg." Initial impressions were "CVA, myocardial infarction, aspiration pneumonitis, possible TUR syndrome." Lumbar puncture, electrocardiogram and chest x-ray were normal. Venous pressure was 20 mm. H20. Serum sodium at this time was 130 meq/L. Twenty-four hours after the acute episode (48 hours after surgery) the patient was dramatically improved: oriented, fully responsive but lethargic. BP was 140/88, pulse 88, respiration 22, temperature 100. Lungs were clear. During the next 15 hour period, urinary output averaged 330 cc/hr., at times going as high as 495 cc/hr. Seventy-two hours after the acute episode (96 hours after surgery), serum sodium concentration was 137 meq/L. Following this, the patient made a slow but steady recovery. It was 9 days before he walked unaided; he was discharged from the hospital on the eighteenth day after surgery. Hemolysis of blood was not present in any of the daily specimens. SUMMARY

In an attempt to evaluate sodium loss and shifts during transurethral prostatectomy, patients undergoing TUR were tagged with N a 22 and laboratory evaluations made of serum, urine and irrigating solutions. The postoperative findings were 1) a decrease in serum sodium, 2) a significant loss of sodium in the irrigating solutions, 3) a decrease in the specific activity (N a22 /N a23 ) of the serum and

FLUID A::\D l,;LECTROLYTE ALTER.\.TIO~S DUHI::\G THANSFRE'I'HR.\L RESECTIOJ'i

4) an apparent innease m the exchangl'able wciiun 1 (N aE). mobilized from Sodium is apparently previously inert bone stores to combat the extrnccllular hyposmolarity whirh leads to the TUR synrlromc. On hoth an experirnental and a clinical basis,

hypertonic (5 per cent) saline is a sournl and f'ffr1> tive "method-of-choice" treatment for tlw Il. ~yndrome. The cmtbors wish to express their to PFC Arnold Plata for hrn tireJes~ efforts ,md outstanding workrna.nship iu performing tbe determinations.