Fluid Therapy in Surgical Emergencies Including Hemorrhage, Loss of Gastrointestinal Fluids, and Thermal Burns

Fluid Therapy in Surgical Emergencies Including Hemorrhage, Loss of Gastrointestinal Fluids, and Thermal Burns CHARLES L. FOX, M.D. * SIGMUND E. LASKER, M.S. **

THE general management of surgical emergencies requires alert, skillful and rapid administration of fluids in addition to the necessary surgical maneuvers. Fluid therapy may be necessary to revive the patient prior to surgery or to combat shock during or after extensive operations. The fluid therapy of surgical emergencies is grouped into four categories: (1) fluid loss is primarily vascular, (2) fluid loss is primarily extravascular, (3) fluid loss is primarily an internal redistribution resulting from tissue injury, and (4) combinations of (1) and (3). VOLUME AND COMPOSITION OF BODY FLUIDS

Knowledge of the volume and composition of body fluids is a prerequisite to successful fluid therapy. Monographs by Gambleu" b cover this subject thoroughly; for the reader's convenience a brief resume follows. Approximately two-thirds of the body is composed of water divided between the fluid within the cells-intracellular fluid (ICF)-and the fluid surrounding Based upon the literature, experimentation in the Surgical Research Laboratory, and clinical studies in collaboration with Drs. J. M. Winfield, W. L. Mersheimer, W. F. Ruggiero and the staffs of the Departments of Surgery, New York Medical College, Flower and Fifth Avenue Hospitals, and the Metropolitan Hospital, New York, N. Y. Aided by Grant RG-2970, Division of Research Grants, Department of Health, Welfare and Education.

* Research Associate (Professorial Rank) in Surgery and Associate in Physiology, New York Medical College; Assistant Surgeon, Flower and Fifth Avenue Hospitals; Associate Surgeon (Pathological Physiology), MetropolitanHospital. ** Research Chemist, Department of Surgery, New York Medical College, Flower and Fifth Avenue Hospitals. 335

Charles L. Fox, Sigmund E. Lasker

336

the cells-extracellular fluid (ECF) (Fig. 91). The largest component of body water, intracellular fluid, is the site of the vital metabolic activities of the body. The intracellular cations: potassium, magnesium and hydrogen, and anions: phosphates and bicarbonates, * regulate the functioning of its enzymes. EXTRA-

INTRACELLULAR

CELLULAR FLUI D S

...

~:E

, 20% ,

FLUIDS

B. w.

14 L.

~

50%

BODY WT.

35 LITERS

XHCO;

+

No+

No

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

2,700 mEq.

Mg*

01

K+

K+

-

HOO 3 ~-_ -_ =)= 9[':-_ -_ ==== R-P0 4-

3,000 mEq.

Mgit

Co'"

PROTEINATE-

p=

Fig. 91. The size and composition of the body compartments, which are drawn to scale. The plasma comprises approximately one-fourth of extracellular fluid. The heavy broken line represents the cell barrier between intracellular and extracellular fluid. The chemical components are shown in areas that approximate their magnitude. The plasma is the smallest fraction of body fluids, amounting to 5 per cent of body weight and approximating one-quarter of the extracellular fluid. The remaining three-quarters of the extracellular fluid is the interstitial fluid which lies outside of the vascular compartment and intimately surrounds the cells of the body. Interstitial fluid is the vehicle for transport of oxygen, carbon dioxide, solid nutrients and waste materials. It also provides an environment of regulated ionic composition-hydrogen ion concentration and osmotic pressure-thereby controlling cell hydration. Interstitial fluid and plasma, the components of extracellular fluid, are similar in chemical composition, but intracellular fluid is entirely different (Figs. 91, 92). Nevertheless, the osmotic pressures of both fluids, indicated in the figure by the heights of the columns for positive and negative ions, are approximately equivalent (Fig. 92).

* The word "bicarbonate" as used here and later refers to the carbon dioxide content or combining power of plasma or tissues as measured by the Van Slyke method. Symbol: HCO.-.

337

Fluid Therapy in Surgical Emergencies

Other body fluids are compared in Figure 92 with extracellular fluid; all contain higher concentrations of potassium, the dominant cation of intracellular fluid. The low level of potassium in predominantly sodium-containing extracellular fluids contrasts sharply with the low level of sodium in predominantly potassium-containing intracellular fluid. The balance and distribution of the fixed cations (sodium and potassium) and the fixed anions (chloride and phosphate) play major roles in regulating the composition and the volume of the body fluids. l .! 400

t

1-----.

,UNDETER·

...' .

mEq/L

375

.MINEDI

,, , ,

1----..1

350

UREA

BODY COMPARTMENTS

GASTRO-INTESTINAL SECRETIONS

pH &.4

JUrCE

MUCUS

ATI C

NaCI

LOlrc

LACTATE

TONIC

IALANCED (DAIUIOW) IUTLER

3.5 L.

15 L.

35 L.

Fig. 92. Comparison of body fluids, secretions and replacement solutions. Plasma, interstitial fluid, gastrointestinal secretions and physiological replacement solution are similar; acid urine contains sodium and chloride like the plasma. The high potassium concentration of intracellular fluid contrasts with the low potassium concentration of all other body fluids. Bicarbonate (HCOs) is a prominent constituent of these fluids except acid urine and acid gastric juice, and is provided in replacement solution by metabolism of acetate or lactate. (The varying widths of the columns are of no significance; the heights of the columns indicate the concentrations in mEq./L. of each constituent.

The dependent interrelationships disclosed by these diagrams help clarify how a major change in one compartment (for example, reduction in vascular volume) results in prompt and profound alterations in both interstitial and intracellular fluids. Full appreciation of this implication makes it obvious that "replacement of vascular volume" only, neglects the requirements of the vastly larger and important extravascular and cellular compartments. Replacement and Repair Solutions

Replacement solutions are compared in Figure 93. "Normal saline," 0.9 per cent sodium chloride, differs from body fluids in containing excess chloride and lacking several essential components. Used in large amounts it has caused many dangerous translocations of electrolyte and fluid. 3 Because of its shortcomings,

Charles L. Fox, Sigmund E. Lasker

338

its use has been restricted and dextrose and water advocated. This substitution ignores the fundamental fact that body fluids contain water and electrolytes, and both need to be replaced. It has long been known that intracellular as well as extracellular fluid may be lost in various conditions causing dehydration. It has also been known that infusion of sodium chloride is followed by loss of intracellular potassium-the COMPARISON

OF BALANCED ELECTROLYTE (ALL CONCENTRATIONS

NORMAL PLASMA

B. E.S. (FOX)

SOLUTION. PLASMA

AND

OTHER

SOLUTIONS

IN MILLI. EQUIVALENTS PER LITER I

0.9% NaCI

MIS SOOIUM LACTATE

RINGER

HARTMANN

OARROW

NaCI PLUS KCI

No

140

140

154

167

147

1~8

122

110

CI

103

103

154

0

157

112

104

140

HC03

27

55'

0

167'

0

36·

53·

K

5

10

0

0

4

5

35

30

Co

5

5

0

0

6

3

0

0

MQ

3

3

0

0

0

2

0

0

HCO,

YIELOEO

BY

METABOLISM

OF ACETATE

OR

.

0

LACTATE.

Fig. 93. Composition of replacement solutions. Comparison of the electrolyte content of replacement solutions with plasma is informative. Sodium is low in some, high in others, some contain excess chloride instead of bicarbonate. Many lack potassium, and calcium and magnesium are also frequently lacking. The physiological balanced solution contains twice the plasma level of potassium and bicarbonate (as precursor) because these two are usually needed; the other ions of the plasma are present in normal concentration. B.E.S., balanced electrolyte solution.

Bunge phenomenon. 1b Nevertheless, potassium was not added to a repair solution because of the hazard of harm to the heart. Darrow4 demonstrated that potassium can safely be used by replacing about one-fourth of the sodium in Hartmann's salt lactate solution by potassium. This produces a concentration of potassium about eight times that of extracellular fluid. After infusion of Darrow's solution, some potassium is removed by the kidney, but most of it goes rapidly across to the intracellular compartment without causing a dangerous increase of concentration in extracellular fluid en route. 1b Comparison of Darrow's solution with the NaCl+KCl solution (last column, Fig. 93) discloses the problems created by adherence to chloride as the sole anion. For replacement of intracellular loss, potassium should be covered by an oxidizable anion, acetate or lactate, rather than chloride.1b Because of the possibility that under certain circumstances 40 mEq.jL. of potassium might be unsafe, Darrow has advocated dilution of his solution with dextrose in water.

Fluid Therapy in Surgical Emergencies

339

With these considerations and based on the surmise that advancing knowledge may disclose the importance of calcium and magnesium replacement, the physiological balanced electrolyte solution depicted in Figures 92 and 93 was compounded and tested. s (Phosphate is omitted because it precipitates with calcium.) The body handles this solution differently than saline, the potassium concentration of 10 mEq.jL. has not proved toxic and plasma ratios of Cl to HC03 are adjusted toward normal. 6 This solution* can be approximated by mixing together 1000 cc. of 0.9 per cent sodium chloride and 500 cc. of M/6 sodium lactate, and then adding from available ampules 15 mEq. of potassium chloride, 7.5 mEq. of calcium gluconate and 4.5 mEq. of magnesium sulfate. Dextrose may conveniently be added to electrolyte solutions for the purpose of providing calories and thereby sparing protein. Incidentally, both potassium and sodium are also conserved. 1a In patients restricted to parenteral therapy, up to 3 grams per kilogram of body weight per day are effective. Solutions containing 5 or 10 per cent carbohydrate in addition to electrolyte should be given intravenously. WHEN FLUID LOSS IS PRIMARILY VASCULAR

Surgical emergencies in which the fluid loss is primarily vascular include massive hemorrhage from traumatic or surgical lacerations of the great vessels or heart, postpartum hemorrhage, rupture of varices or aneurysms, or profuse gastrointestinal bleeding. Pathological Physiology of HenlOrrhage

Massive loss of blood reduces rapidly the volume of blood in the vascular bed. Blood pressure falls precipitously; blood vessels, especially capillaries, become constricted. The rate of the heart increases but stroke volume and cardiac output decrease to a fraction of normal resulting in profound biochemical and physiological changes throughout the body. 7 The pathognomonic symptoms of shock then appear. The pulse becomes rapid and weak and the extremities feel cold. Respirations increase in both depth and frequency as the hyperpnea of acidosis develops. (Hyperpnea is initiated by acidosis, not by oxygen lack, inasmuch as the respiratory center is far more sensitive to changes in carbon dioxide tension and pH than to oxygen lack). Body temperature falls as cellular metabolism is impaired. Urine formation is halted. Loss of consciousness ensues. Biochelllical Changes in Helllorrhage

The reductions in blood volume and blood pressure initiate progressive biochemical changes. The fall in capillary pressure reduces filtration outward and the relatively unopposed plasma colloid osmotic pressure draws interstitial fluid into the vascular bed. The combination of reduced blood pressure; decreased cardiac output and vasoconstriction lead to capillary stasis and stagnant anoxia as transfer of oxygen to cells via interstitial fluid is halted. The critical role of interstitial fluid is empha-

* The balanced electrolyte solution was prepared and generously supplied for our studies by the Cutter Laboratories, Berkeley, California, Dr. Walter E. Ward, Medical Director.

340

Charles L. Fox, Sigmund E. Lasker

sized by the finding that a normally trivial blood loss may cause death when interstitial fluid is depleted. 8 Inadequate oxygenation of cells prevents their normal metabolism; instead, anaerobic reactions dominate, leading to formation of phosphoric and other acid metabolites, cellular acidosis, splitting of organic comTable 1 PHYSIOLOGICAL AND BIOCHEMICAL CHANGES IN EXPERIMENTAL HEMORRHAGIC SHOCK: EFFECTS OF THERAPY WITH SODIUM SOLUTION . AFTER CONTROL

Blood pressure (mm.) ............... . 90 Heart rate (per min.) .............. . 90 43 Hematocrit (%) Plasma protein (gm./lOO mI.) ....... . 5.8 Arterial oxygen (vol. %) ........... . 18 Mixed venous oxygen (vol. %) ...... . 14 A-V difference ..................... . 4 Cardiac output (cc./min./kg.) ....... . 274 Stroke volume (cc.) ................ . 30 pH ............................... . 7.3-4 pCO-;; (mm. Hg) ................... . 40 Bicarbonate (mEg./L.) ............. . 25 Phosphate (mEg./L.) .............. . 1.4 Lactate (mEg./L.) ................. . 2 Pyruvate (mEg./L.) ............... . 3 110 Chloride (mEg./L.) ......... . 4 Potassium (mEg./L.) ....... . Nonprotein nitrogen (mg./lOO m!.). 28

HEMORRHAGIC

RECOVERY AFTER INFUSION OF

SHOCK

SODIUM SOLUTION

30--40 190-250 39 5.2 16

95 120 9.2

4

12 74

2 9

5 4

265

2

7.0-2 7 3

9.7 15

7.4

20 1.5

10

109 5* 60 (anuria)

105

2

* May rise to 10-15 just before death. Data compiled from Gregerson7, Reynolds1o and Fox et al. 5 These data show that the loss of intravascular volume by hemorrhage is followed by significant physiological and biochemical alterations.

plexes into numerous ionic particles and release of potassium. The major blood changes show the development of severe acidosis: pH falls while phosphate, lactate and pyruvate and amino acid nitrogen rise; bicarbonate falls progressively as fixed acids are formed and combine with the base of bicarbonate. Representative measurable changes occurring during hemorrhagic and traumatic shock are surveyed in Table 1, columns 1 and 2. Most of these changes occur progressively but this is not true of the blood volume, which is reduced rapidly during the hemorrhage. Thereafter not only blood volume but the hematocrit and plasma protein values remain essentially unchanged. 7 In experimental hemorrhage, potassium equivalent to from 10 to 20 per cent of total body potassium was found in the large volumes of urine excreted after infusion of sodium salt solutions." Plasma potassium levels decreased also.

Fluid Therapy in Surgical Emergencies

341

Ai!, a result of these events the blood volume is reduced by the amount of blood lost minus the fluid transferred from the interstitial compartment. The volume of interstitial fluid is reduced both by the transfer of interstitial fluid into the hypotensive vascular space and the imbibition of interstitial fluid water by anoxic, acidotic tissue cells. The ultimate consequence of alterations in all the body compartments is the progressive decrease in cardiac output which may fall to a level where death occurs.

Therapeutic Considerations

The objective of therapy is to restore cardiac and renal output and the function of other vital organs so that essential surgical procedures can be performed. If the vascular compartment were an inflexible system of rigid pipes and if 3 liters of blood were lost from such a system containing 7 liters, 3 liters of blood would presumably refill the system and achieve complete restoration of vital functions. The vascular compartment, however, is quite different: it is a flexible system of vessels which constrict and dilate; the walls of these vessels are semipermeable and are suspended in the interstitial fluid which surrounds the tissue cells. Following loss of 3 liters of blood from the vascular bed, interstitial fluid enters and extracellular and intracellular alterations are initiated. Because of these rearrangements it is not to be expected that transfusion of the amount of blood lost will re-establish the original blood volume. Actual measurements after transfusions of the red cell volumes (using chromium 51 tagged erythrocytes) and plasma volumes (using p3i labeled albumin) revealed changes in blood volume different than the volumes transfused. 9 The complex events that follow massive hemorrhage suggest that complete restoration with return of renal function involves not only blood replacement but also repair of both interstitial and intracellular components. The keynote of successful therapy is speed and adequate volume. Blood is vital; when not immediately available, plasma expanders such as 6 per cent dextran in saline can be used without delay for typing. In the past, solutions of sodium salts have been relegated to a minor role because "they do not stay in the circulation" and also run out through the kidneys. More complete understanding of the mechanism of hemorrhagic shock emphasizes that these constitute important reasons for utilizing, even when adequate supplies of blood are freely available, electrolyte solutions which contain not only sodium chloride, but also potassium, calcium, magnesium and bicarbonate ions-the physiological, balanced electrolyte solution depicted in Figures 92 and 93. When this solution is infused, a portion remains in the vascular system, overcoming capillary stasis and expanding the blood volume; another portion rapidly passes out of the vascular tree and refills the interstitial compartment. Replacement of interstitial fluid restores normal transport of oxygen, carbon dioxide, and other vital metabolites between the blood

Charles L. Fox, Sigmund E. Lasker and the tissue cells. As a result, cardiac output becomes normal despite the marked anemia (low hematocrit) and hypoproteinemia (Table 1, column 3). With normal cardiac output, the A-V oxygen difference becomes normal, cellular anoxia and acidosis are overcome, and renal function is revived. 10 The improvement in renal function is apparent as much of the infused sodium and water are excreted. Although one might anticipate maximal adrenocortical response with sodium retention because of the severe stress imposed by profound hemorrhage,' infusion of sodium salts is followed by rapid excretion of two-thirds of that administered. This diuresis, characterized by the potassuria cited above, 5 is in marked contrast to the oliguria that frequently follows therapy with blood alone. The biochemical and physiological improvements cited may be the underlying basis for the immediate therapeutic benefit of sodium salts alone in severe experimental hemorrhage. 10 , 11 Dosage of Therapeutic Agents and Criteria of Adequacy

Profound shock results when approximately one-half of the vascular volume has been lost. 7 , 10, 11, 12 Inasmuch as the vascular volume constitutes 7 to 9 per cent of body weight (70 to 90 cc. per kg., or 35 to 45 cc. per pound of body weight), transfusion of 2500 to 3200 cc. of blood with great rapidity might be necessary. In addition, tissue fluid replacement and occasionally additional electrolyte solution for correction of the acidosis are required. To meet all indications, therapy should be supplemented by from one to three times as much balanced electrolyte solution administered promptly before, during and after replacement of the blood estimated to have been lost. When blood is not freely available, larger amounts-from 100 to 150 cc. per kg. body weight-of electrolyte solutions given rapidly may be life-saving. 10 , 11 Blood pressure is a notoriously unsafe guide to therapy; when hypotension persists and there is a possibility of overloading the vascular compartment by administering too much blood, balanced electrolyte solutions with their larger volume of distribution are effective and safer. Inadequate volume and low concentrations of sodium in the urine signify a need for more replacement of extracellular fluid. Infusion of electrolyte solution and establishing good urine output carry less hazard than the risk of overloading the circulation with excess blood. After severe hemorrhage, plasma bicarbonate may be reduced to the vanishing point-less than 5 mEq./L. Because of the deleterious effects of severe cellular acidosis, correction is desirable; for this purpose isotonic sodium salt solutions should be used; the inefficacy of hypertonic sodium bicarbonate solutions was demonstrated. 12 According to the Van Slyke formula, from 1 to 3 liters of M/6 or preferably M/7 isotonic sodium lactate may be necessary.13 Guides to dosage are repeated determinations of the plasma bicarbonate and slowing of respirations to normal. Bank blood is of slight value in combating acidosis; each 500

p

Fluid Therapy in Surgical Emergencies cc. of ACD blood contains sodium citrate equivalent to 125 cc. of an isotonic solution. Dextrose in water is contraindicated; it proved of no value in experimental hemorrhage,l1 probably because of failure to expand intravascular or extracellular fluid volumes. In experimental hemorrhage, potassium concentrations of 10 mEq./L. in the sodium salt solutions were needed to maintain plasma potassium at normal. This added potassium compensated for that excreted in the urine, perhaps by preventing sodium-potassium exchange in cells, and seemed to reduce both the tachycardia and the volume of infusion needed to prevent circulatory collapse. s Accordingly, in the management of severe hemorrhage the sodium salt solutions utilized should contain 5 to 10 mEq./L. of potassium. (It would also seem desirable to include potassium and other ions of the extracellular fluid in plasma expander solutions.) Vasopressor agents such as norepinephrine may occasionally prove helpful in combating hypotension. During profound hemorrhage, infection causing bacteremia or toxemia may occur. Although doubt prevails as to their clinical significance, prevention by generous use of antibiotics is warranted. Possible COIllplications of Therapy of HeIllorrhage

Pulmonary Edema. Its exact etiology is unknown but when this complication follows blood or plasma transfusions approximating or exceeding one-half the patients' normal blood volume, excess administration must be suspected. Pulmonary edema and congestive atelectasis occurred in patients who received large volumes of glucose in water with and without mUltiple transfusions. 14 When the source of the hemorrhage cannot be located and continuous bleeding is suspected, additional blood in excess of half the blood volume should be administered only after careful consideration of the possibility of overloading the circulation. Renal Shutdown. Protracted renal ischemia leads to irreparable damage of renal cells. 1sa , b Experimental hemorrhage treated with electrolyte solutions is characterized by copious urine flow starting long before the blood volume is restored to normal. 10 Presumably the resulting expansion in extracellular volume activates the kidney via its role in regulation of extracellular volume. Prompt infusion of large amounts of electrolyte solution after hemorrhage, fluid loss, trauma or burns may prevent renal ischemia. When renal damage has occurred, extreme caution and restraint in fluid therapy are essential. Routes of AdIllinistration

Arterial infusion utilizing a pump has been suggested; equivalent volumes rapidly administered intravenously, however, were equally effective. When the patient is in profound collapse and veins or arteries

Charles L. Fox, Sigmund E. Lasker need to be cannulated, immediate intraperitoneal administration of physiological electrolyte solution may be life-saving. Subsequently, when a vein or artery is cannulated, blood or colloid can be given simultaneously. Finally, subcutaneous, intramuscular and oral administration of electrolyte solutions should not be overlooked. Aspiration must be prevented if vomiting occurs; use of a nasogastric tube is helpful. WHEN FLUID LOSS IS PRIMARILY EXTRAVASCULAR

The second type of surgical emergency characterized primarily by losses of extravascular fluid includes vomiting due to pyloric obstruction or intestinal obstruction; diarrhea caused by acute inflammation, specific or nonspecific, diverticulitis or neoplasms involving the large or small bowel. Especially serious is the acute, fulminating diarrhea which may follow surgical procedures-presumably an enteritis caused by antibiotic resistant micro-organisms. In addition, the occurrence of fistulas following surgical procedures may lead to rapid and serious depletion. Finally, pancreatitis and peritonitis are characterized by the extravasation of large volumes of fluid into the peritoneal cavity. Pathological Physiology

The electrolyte composition of the gastrointestinal secretions is shown in Figure 92 for comparison with plasma. The secretions contain from two to eight times more potassium. Gastric juice usually contains less sodium than chloride and no bicarbonate; in pancreatic or jejunal fluid, as in plasma, sodium is greater than chloride with bicarbonate making up the difference. After vomiting, loss of chloride from the plasma is made up in part by increase of bicarbonate. The loss of sodium, however, is not so readily replaceable and moreover involves a loss of equivalent anion. Loss of chloride does not deplete the ionic content of the plasma whereas loss of sodium removes both cation and anion, doubly depleting the plasma. lc In many patients the external losses involve mixtures of several portions of the gastrointestinal tract so that similar amounts of sodium and chloride are removed. The loss of sodium from the body is the essential factor in the rapid dehydration that follows loss of these secretions. In addition, varying amounts of potassium, chloride, bicarbonate, calcium and magnesium are lost. As shown in Figure 94 from Gamble's classic studies of pyloric obstruction, progressive decrease in plasma sodium (total base) occurs and is accompanied by a relatively greater loss of chloride and an increase in bicarbonate. 1c Besides the loss of sodium from the plasma, other factors prevent the increase in bicarbonate from equaling the fall in chloride. One factor apparently is the increase in organic acids indicated by the column labeled "R." This factor may also be responsible for the sur-

p

Fluid Therapy in Surgical Emergencies

345

prisingly small increase in plasma alkalinity despite a very large increase in bicarbonate. In addition to loss of potassium via the gastrointestinal fluids, a "mysterious" loss of cellular potassium occurs ;1" potassium is excreted in the urine. As sodium potassium and water are lost, interstitial fluid is sacrificed, thereby minimizing reduction in the volumes of plasma and intracellular fluid. Body weight falls and continuing dehydration causes hematocrit and plasma protein levels to increase. Removal of extracelluPYLORUS OBSTRUtTED I

I

-----,fIhj$.----

1"-."IITT'I'r'~----- 2.~ fii~-------lc5 hi6~- -

100

80

~+--Ht~I~~--··-iHtH~~*-··-Ht OL-llW~~~~~~~~~~WW~~

Fig. 94. Plasma electrolyte changes after pyloric obstruction. Normal plasma on left. Plasma bicarbonate increases as vomiting and loss of chloride continue. Loss of chloride greater than gain in bicarbonate, which may be limited by increase in "R." Most significant change is loss of base-sodium-leading to hypotonicity.10

lar fluid impairs the efficiency of the circulatory system and interferes with exchange of metabolites between cells and their environment. Thitl leads to cellular anoxia and metabolic acidosis with production of organic acids ("R," Fig. 94) and release of cellular potassium. A serious consequence of these events is that renal mechanisms become unable to regulate efficiently the composition and volume of body fluids. Impairment of kidney function at the time it is most essential makes body composition dependent upon the fluid administered. Thus, administration of water or glucose in water accentuates the hypotonicity_ Chenlical Changes in Blood and Urine; Physiological SYnlptOnlS

The chemical changes in the blood and urine may at first glance appear to be variable; thus the plasma chloride, and inversely, the plasma bicarbonate levels, may be above or below normal; depending upon the anatomic location of the gastrointestinal lesion and the degree of acidosis

--

----------

---

Charles L. Fox, Sigmund E. Lasker generated by the electrolyte and fluid loss. However, the positive ion associated with both these anions is sodium, which -decreases in plasma (Fig. 94), and may virtually disappear from the urine although chloride excretion may continue. Plasma potassium may be low or normal; nevertheless, considerable potassium may be excreted continuously in the urine. The development of potassium depletion of sufficient severity to cause hypotension is a possibility.I6 The hematocrit and plasma levels vary too much to be helpful initially. The respiratory rate may be normal or rapid, depending upon the degree of acidosis; slow respirations indicative of compensated alkalosis are uncommon despite the frequent occurrence of elevated plasma bicarbonate levels. Therapeutic Considerations

The primary indication is to administer large volumes of isotonic electrolyte solution containing sodium, potassium, calcium, magnesium, chloride and bicarbonate for the purpose of restoring to normal the volume and composition of the extracellular fluid and to permit gradual replacement of intracellular losses. Large volumes in these patients may mean from 100 to 150 cc. per kg. body weight in the first 24 hours; desperate situations, such as protracted vomiting, or persistent diarrhea as in acute enteritis following operation, may require 1 liter per hour for the first seven hours. The volume of fluid which may be lost from the gastrointestinal tract is enormous; losses three times the plasma volume have been measured. All solutions used should contain potassium. Initially 10 mEq./L. is safe and effective; subsequently, when vascular and extracellular compartments have been expanded, additional potassium is essential for intracellular replacement. When plasma chloride is high and bicarbonate is low, plasma-like solutions are obviously desirable. In contrast, when plasma bicarbonate is elevated and chloride low, three salts, ammonium chloride, sodium chloride and potassium chloride, have been advocated. Gamble found, however, that restoring plasma chloride with ammonium chloride was not beneficial; diuresis with increased losses of potassium and body water resulted. Ie In contrast, sodium chloride might be expected to replace both sodium and chloride in extracellular fluid. This logic is correct except that when potassium deficiency is present, plasma bicarbonate remains high, hypochloremia may persist,17 and extracellular volume may expand after sodium chloride infusions. Since the major loss of sodium in these patients is external, the use of potassium chloride may correct the potassium deficit and elevate plasma sodium only to the extent that sodium has migrated into cells. 2 Likewise, after loss of intracellular fluid by dehydrating processes, potassium chloride was not suitable but potassium acetate was found capable of replacing intracellular fluid. Ib

Fluid Therapy in Surgical Emergencies

347

Ionic shifts between the various body compartments are complex and frequently these chloride salts fail to correct abnormalities. A possible explanation might be the unexpected movement of chloride into the extracellular space during potassium deficiency alkalosis and the finding that potassium bicarbonate proved effective in its prevention. 18 Accordingly, it seems preferable to give both the kidney and the body cells every opportunity to make the necessary adjustments by providing a more complete, physiological balanced solution. Following its administration, potassium is retained and surplus sodium is excreted in the urine together with anions either unwanted or present in excess. The use of dextrose in water under these circumstances is contraindicated when subnormal values of plasma electrolyte prevail. In one case report of acute enteritis, 6 liters of dextrose in water, 3 liters of saline, and 40 mEq. of sodium lactate were administered.1 9 The result: plasma levels of 125 mEq./L. of sodium, 86 mEq./L. of chloride and 19.5 mEq./L. of bicarbonate. Electrolyte analyses of the urine (unfortunately too infrequently performed) disclose low concentrations of potassium and sodium during the period of high electrolyte intake, attesting further to the excess of water and deficit of electrolyte that usually prevails. During therapy, the hematocrit and plasma protein levels may decrease below the initial values; these decreases may be temporary until the fluid administered has been distributed throughout the body compartments. When subnormal values persist, blood can be given (5 cc. per kg. per day) to permit restoration to normal without overloading the vascular bed during active fluid replacement. The use of cortisone or ACTH may be indicated if, after full extracellular fluid replacement, hypotension persists and severe potassium depletion is suspected.1 6 However, vigorous potassium replacement is essential and preferable. WHEN FLUID LOSS IS PRIMARILY AN INTERNAL REDISTRIBUTION CAUSED BY TISSUE TRAUMA

Thermal burns, extensive crushing injuries, gas gangrene infections and compound fractures constitute the type of acute surgical emergency characterized primarily by an internal redistribution of electrolyte and fluid rather than external loss. Redistribution of Body Fluids and Electrolytes in Zone of Injury

Within minutes after thermal or crushing injury to tissue, visible swelling occurs as sodium and water accumulate in the zone of injury. Potassium is extruded from the injured cells which acquire sodium. Some chloride moves with the sodium and some phosphates leave the cells with potassium. These characteristic changes occur also after

Charles L. Fox, Sigmund E. Lasker

348

operative trauma, as shown in Figure 95. Depending upon, the nature and severity of the injury, varying amounts of albumin and some red cells may accumulate in the traumatized regions. 9 The water and electrolyte which accumulate in the zones of injury originated in the plasma and interstitial compartments but their volume is small compared to the absorptive capacity of traumatized cells. K

No

(mEq.1

No and K ••pre.sed in mE..per 100 9. fol fr•• dry wI.

H.O

K

No

H.O

(%)

63 mEq, average urine K - 40 hrs. post op.

Fig. 95. Electrolyte and water shifts after tissue trauma. Preoperative and postoperative muscle biopsies of rectus femoris (nontraumatized area) and rectus abdominis (zone of trauma). Traumatized rectus abdominis gained water and sodium, lost potassium. No significant change in nontraumatized tissues. 6

Consequently, when many cells are traumatized, their avidity remains unsatisfied until therapy is begun, whereupon much of the electrolyte and water of administered plasma or electrolyte solutions are transferred to the injured regions. 20 It should be emphasized that the trauma produced the physiochemical changes which cause injured tissues to have such avidity for sodium and water rather than infer that fluid therapy created the influx. Systemic Physiological and Biochemical Changes

The volume and composition of body fluids are profoundly altered by losing much sodium and water to the zones of injury; thus the blood volume may be reduced more than after a fatal hemorrhage 7 and the interstitial fluid content of vital organs is also greatly reduced. 9 The disproportionately larger amount of sodium than water acquired by injured tissues ultimately lowers the plasma sodium concentration. Decreases in the volume and sodium concentration of extracellular fluid

Fluid Therapy in Surgical Emergencies

349

produce physiological alterations similar to those described above: reduction in blood volume, decreased cardiac output, cellular acidosis, and renal failure. When the burn involves the face, the mucous membranes of the respiratory tract frequently become involved; edema of the airways may impede ventilation and thereby accentuate acidosis and increase hyperpnea.

Fig. 96. Plasma electrolyte values of patients in shock from severe burns. Admission value of 12 patients with burns 35 to 50 per cent of body surface area. Bicarbonate is invariably low and usually becomes lower. In contrast, chloride is normal or above. Sodium values vary from above to below normal on admission but, at 72 hours, all were subnormal. Acidosis present initially; hyponatremia in some initially, but in all subsequently.

The changes in blood chemistry are significant. The hematocrit becomes elevated; if concomitant blood loss or red cell destruction occurs, the hematocrit rise is slight. In the plasma, as shown in Figure 96, bicarbonate is reduced, chloride elevated, and sodium, which may be normal initially, decreases thereafter. Urine volume becomes minimal and the sodium and chloride concentrations may diminish to the vanishing point; potassium concentrations increase. Hemoglobin may appear in the urine if extensive red cell destruction occurs. Therapeutic Considerations

The objectives of therapy are to restore cardiac output, replace extracellular fluid, and revive kidney function. The last is essential after crush injury to muscle or gas gangrene because urine is the sole route for removal of potassium extruded from injured tissues. These objectives are achieved by replacing rapidly the sodium and water of the extracellular fluid redistributed in the injured tissues. Replacement of plasma and blood based on estimated losses should follow, but their losses are

Charles L. Fox, Sigmund E. Lasker

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quantitatively less than the losses of sodium and water. The primary therapeutic effort is directed at replacement of the major deficits. Inasmuch as both electrolyte and water are acquired by injured tissues and since subnormal plasma sodium levels occur after extensive burns or other tissue trauma, the inadvisability of administering glucose and water solutions which further lowers electrolyte levels becomes obvious~ Table 2

FLUID THERAPY OF EXTENSIVELY BURNED PATIENTS SURVIVING SHOCK (Full thickness burn in each patient was 35 to 55 per cent of body surface area)

PATIENT AGE

WEIGHT (kg.)

Colloid Therapy Group 6 17 S 20 K 9 E 52 30 D 38 45 72 50 G Sodium Salts Only Group T 4 15 15 De 5 50 82 0

THERAPY IN FIRST 24 HOURS* Sodium Total Colloid

30 40 30 30 10

PI PI PI-Bl Bl Bl

None None None

THERAPY IN FIRST 72 HOURS* Sodium Total Colloid

140 110 70 70 110

170 150 100 100 120

30 60 70 80 10

PI PI PI-Bl PI-Bl Bl

80 130 100

80 130 100

None None None

310 310 130 140 190

340 370 200 220 200

290 250 270

290 250 270

* All values are expressed as cc./kg. body weight. Bl = whole blood; PI = plasma; its average sodium concentration was found to be 190 mEq./L. Data from Fox et a1. 24 Dosage and Guides to Therapy

Various formulas have been proposed for the fluid therapy of extensive burns, but well documented clinical evidence attesting to their efficacy and adequacy is lacking. 1s • 21 Measurements of the acute red blood cell destruction following severe thermal burns in dogs revealed destruction of 8 to 10 per cent of red cells, and Raker and Rovit22 "believe that there may be important danger in providing the burned patient with more red cells than are acutely destroyed, for the increase in viscosity of the circulating blood may be exaggerated by such therapy.... The implications of this study seem clear ... that massive whole blood transfusion therapy of the burned patient is not indicated in the first 48 hours after injury ... It should be emphasized that there is no question of the frequent need for liberal use of whole transfusions during the phase of infection of the burned area and the phase of preparation of the patient for covering of granulating areas." In full thickness extensive burns, as shown in Table 2, the volume of

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fluid required for replacement may approximate one-half the total volume of extracellular fluid and range from 100 to 150 cc. per kg. of body weight within the first 24 hours.l3. 21-26 Initially, the fluid should be administered rapidly by all possible routes-intravenous, subcutaneous, intraperitoneal or oral-depending upon the location of the injury and the condition of the patient. In adults, a liter per hour for the first five to ten hours may be necessary. In view of the reduced bicarbonate and elevated chloride found in the plasma of patients with extensive burns (Fig. 96) and because large volumes of solution are employed, it is advisable to utilize physiological electrolyte solutions that approximate plasma in composition (Fig. 92). Thus, body electrolyte concentrations can be brought to normal with less hazard of overloading or overcorrecting. l3 .25 Precise dosage is impossible because neither the total mass of tissue injured nor the extent of their fundamental chemical changes can be gauged exactly. In practice, effective guides to therapy are primarily the physiological and biochemical response of the patient. When fluid and electrolyte are given as indicated in Table 2, the heart rate and respirations slow to normal; the hematocrit decreases and the bicarbonate increases to normal; the rate of urine formation rises to 50 cc. per hour, and urine sodium concentration reaches 50 to 100 mEq.jL. Further experience with extensive burns has shown that the fluid and electrolyte problems may continue for many days. The best approach now available is to maintain normal values for extracellular and intracellular components. Approximately 1 to 3 mEq. per kg. body weight of both sodium and potassium bicarbonate, or acetate with only 0.5 to 1 mEq. per kg. of sodium chloride daily, will usually maintain the bicarbonate at normal, prevent hyponatremia and replace intracellular potassium. These mineral intakes should supplement a high caloric food intake; excess water intake should be prevented. COMBINATIONS OF FLUID LOSS

Combinations are exemplified (a) by postoperative shock following operative blood loss and tissue trauma, or (b) by gastrointestnial hemorrhage with protracted vomiting or diarrhea. In addition to hemorrhage, these syndromes are characterized by loss of sodium and water from the extracellular fluid, either by redistribution into traumatized tissues (Fig. 95) or by external loss. The combination of loss of vascular volume plus major loss of extracellular fluid seriously reduces cardiac output, thereby leading to stagnant anoxia and cellular acidosis as described above. Depletion of extracellular fluid creates a setting in which a relatively small blood loss results in disproportionately profound shock. 8 This fact is often not realized and erroneously therapy is primarily transfusion for the obvious blood loss; persistent hypotension and "disappearance" of blood may follow. The major therapeutic effort should be

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Charles L. Fox, Sigmund E. Lasker

adequate replacement of extracellular fluid followed by blood as needed to restore red cell volume to normal. Thus, replacement of extracellular fluid expanded blood volume although red cell mass was subnormal. 9 After extensive surgical procedures, from 60 to 100 cc. per kg. of electrolyte solution may be required, followed by 10 to 20 cc. per kg. of whole blood. Subnormal hematocrit and a urine output of 50 cc. per hour are indications for additional blood without electrolyte solution; rising hema tocrit and oliguria are indications for less blood and more electrolyte solution. Overtreating the blood loss and undertreating or disregarding the losses of extracellular electrolyte and fluid may lead to hypotension, pulmonary edema and oliguria. SUMMARY

The various types of fluid and electrolyte disturbances which may occur in surgical emergencies are described and integrated with a review of the interrelationships of body compartments. The pathological physiology, symptomatology and rationale of therapy with laboratory guides have been set forth in an effort to emphasize the total picture. Much remains unknown but a wider understanding of what is known can prove extremely helpful. REFERENCES 1. (a) Gamble, J. L.: Chemical Anatomy, Physiology and Pathology of Extracellular Fluid. Cambridge, Mass., Harvard University Press, 1951. (b) Gamble, J. L.: Lane Medical Lectures. Companionship of Water and Electrolytes in the Organization of Body Fluids. Stanford, Cal., Stanford University Press, 1951. (c) Gamble, J. L. and Ross, S. G.: The Factors in Dehydration. J. Clin. Investigation 1: 403, 1925. 2. Cooke, R. E. and others: The Role of Potassium in the Prevention of Alkalosis. Am. J. Med. 17: 180, 1954. 3. Coller, F. A. and others: Translocation of Fluid Produced by Intravenous Administration of Isotonic Salt Solution in Man Postoperatively. Ann. Surg. 122: 663,1945. 4. Darrow, D. C.: Therapeutic Measures Promoting Recovery from the Physiologic Disturbances of Infantile Diarrhea. Pediatrics 9: 519, 1952. 5. Fox, C. L. Jr. and others: Electrolyte Solution Approximating Plasma Concentrations. J.A.M.A. 148: 827, 1952. 6. Winfield, J. M., Fox, C. L. Jr. and Mersheimer, W. L.: Etiological Factors in Postoperative Salt Retention and Its Prevention. Ann. Surg. 134: 626, 1951. 7. Gregersen, M.: Shock. Ann. Rev. Physiol. 8: 335, 1946. 8. Gilman, A.: Experimental Sodium Loss Analogous to Adrenal Insufficiency: The Resulting Water Shift and Sensitivity to Hemorrhage. Am. J. Physiol. 108: 1934. 9. Fox, C. L. Jr., Lasker, S. E., Winfield, J. M. and Mersheimer, W. L.: Albumin, Potassium, Sodium and Chloride Redistribution and Erythrocyte Loss after Surgical Trauma and Extensive Burns. Ann. Surg. 140: 524, 1954. 10. Reynolds, M.: Cardiovascular Effects of Large Volumes of Isotonic Saline Infused Intravenously into Dogs Following Severe Hemorrhage. Am. J. Physiol. 158: 1949. 11. Rosenthal, S. M. and Tabor, H.: Electrolyte Changes and Chemotherapy in Experimental Burn and Traumatic Shock and Hemorrhage. Arch. Surg. 51: 244, 1945.

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12. Wiggers, C. J.: Physiology of Shock. New York, The Commonwealth Fund, 1950, p.340. 13. Harkins, H. N. and others: Fluid and Nutritional Therapy of Burns. J.A.M.A. 128: 475, 1945. 14. Jenkins, M., Jones, R., Wilson, B. and Moyer, C. A.: Congestive Atelectasis-A Complication of Intravenous Infusion of Fluids. Ann. Surg. 132: 327, 1950. 15. (a) Van Slyke, D. D.: The Effects of Shock on the Kidney. Ann. Int. Med. 28: 701, 1948. (b) Oliver, J., MacDowell, M. and Tracy, A.: The Pathogenesis of Acute Renal Failure Associated with Traumatic and Toxic Injury; Renal Ischemia, Nephrotoxic Damage and the Ischemuric Episode. J. Clin. Investigation 30: 1305, 1951. 16. Freed, S. D., Rosenman, R. H. and Friedman, M.: The Relationship of Potassium in the Regulation of Blood Pressure with Special Attention to Corticosteroid Hypertension. Ann. New York Acad. Sc. 56: 637, 1953. 17. Ariel, 1. M.: Effects of Acute Hypochloremia on Distribution of Body Fluid and Composition of Tissue Electrolytes in Man. Ann. Surg. 140: 150, 1954. 18. Roberts, K. E., Randall, H. T., Philbin, P. and Lipton, R.: Changes in Extracellular Water and Electrolytes and the Renal Compensations in Chronic Alkalosis, as Compared to Those Occurring in Acute Alkalosis. Surgery 36: 599,1954. 19. Christianson, C. S., Dacquisto, M. P. and Dobbs, W. H.: Micrococcic (Staphylococcic) Enteritis: Recovery Following Shock. Gastroenterology 26: 645, 1945. 20. Koletsky, S. and Gustafson, G.: Tourniquet Shock in Rats. Am. J. Physiol. 229: 178, 1954. 21. National Research Council: Symposium on Burns. National Academy of Science, 1950. 22. Raker, J. W. and Rovit, R. L.: The Acute Red Blood Cell Destruction Following Severe Thermal Trauma in Dogs. Surg., Gynec. & Obst. 98: 169, 1954. 23. Fox, C. L. Jr.: Oral Sodium Lactate in the Treatment of Burn Shock. J.A.M.A. 124: 207, 1944. 24. Fox, C. L. Jr., Mersheimer, W. L., Lasker, S. and Winfield, J. M.: Comparative Experimental Studies on the Treatment of Traumatic Shock. Am. J. Surg. 85: 359, 1953. 25. Fox, C. L. Jr. and others: Observations of the Effects of Blood Plasma and Sodium Salts on the Treatment of Extensive Full-Thickness Burns. Am. J. Surg. 1955 (in press). 1249 Fifth Avenue New York 29, N. Y.