340 LETTERS TO THE EDITOR Metcoff deplored the use of “rather arbitrary
formulae” to simplify the prevention of shock
in burned patients, yet stated they were based
on careful study by Evans et al. and the Brooke
Army Group-and on certain assumptions. He
says that use of these formulae results in the
administration of too much water, sodium, and
protein, yet he admits that “the most important
cause of death after severe burns is the de-velopment of infections in the second post-burn week,” not shock or poorly treated shock.
He uses figures from an earlier paper (New
Eng. I. Med., July 2, 1962) by him and several
colleagues to support his contention of
over-hydration, when in the derivation of these
fig-ures, no account was taken of the fluid lost at the time of admission debridement before ad-mission of the patients to the Metabolic Unit
for balance studies, and where the edema fluid
in the burned area is determined by “some
theoretical estimates” to be 2.8 ml/100 cm of burned area, a figure which seems absurdly
small to one who has witnessed the burn
caused puffiness of face and hands and
meas-ured the urine voided during the period of
diuresis. Using this figure, the ratio of fluid
loss by exudation to that lost to edema (through
the wound: into it) is calculated at slighfly less
than 3 : 1. Ever since Cope and Moore (Ann.
Surg., 126:1010, 1947) demonstrated the
se-questration of fluid in the burn wound, there has been general acceptance of the concept
expressed as follows by Reiss et al. (J.A.M.A.,
152:1309, 1953): “The exudate that weeps so
copiously from the surface of a recent partial
thickness burn is but a small fraction of the
total loss : the ma/or loss occurs in the tissues and is concealed from vision until the wound begins to swell a few hours after injury. In full
thickness burns, visible exudation is completely
absent.”
This premise of fluid loss into the wound and
through it as a cause of hypovolemia is one of
three assumptions which Dr. Metcoff says is
“largely incorrect.” He is critical of the use
of hematocrit determinations and volume of
urine output as guides to fluid therapy, but
offers nothing in their place and distorts the usual practice by using the word “normal”
(pre-determined urine volume) when “minimal” is
the more accurately descriptive term. His third
assumption that “generalized edema is a conse-quence of the pathology of bums” is a straw
man as far as the undersigned is concerned.
Dr. Metcoff states further that the “quanti-ties of potassium provided by the usual repair fluids appear to be inadequate” and then pre-sents evidence of considerable diminution of
renal function-a contraindication to the
ad-ministration of potassium. He worries about the indwelling catheter as a source of blood stream infection when all he has to do is culture his
burn wounds for evidence of a much more
likely source of organisms.
Finally Dr. Metcoff appears to be concerned
that urine output does not reflect fluid input
when the reason for giving fluid is to satisfy the losses into and through the burn wound,
thus preventing further hvpovolemia and
hemoconcentration, and not to flush the
kid-neys!
Bums look big. It is a common house officer error to estimate a burned area at 25 to 50% more than it actually is. When such unrealistic figures are used in a formula, the patient will get 25 to 50% more fluid than he should. (Ac-tually, best results are obtained by using a formula as a springboard only, modifying the amount of water, electrolyte, and protein infu-sion in accordance with clinical and biochemi-cal observations-but not “measured losses of sodium, water, and electrolytes from the burned surface”!!)
So it seems to this user of a formula for planning fluid therapy in burned patients that Dr. Metcoff has attempted to take away much while offering little of practical value in return
and that until his arguments are less
contradic-tory, better supported, and more “simply” pre-sented, he won’t get away with it.
J
OHN CHAMBERLAIN, M.D. Brookline, MassachusettsEDITOR’S NOTE: Dr. I’Ietcoff’s comment upon Dr.
Chamberlain’s letter follows.
To ThE EDITOR:
Dr. Chamberlain is an experienced pediatric
surgeon with an extensive practical knowledge
of surgical treatment in children. In his
com-mentary on my Commentary on Burn Therapy
(PEDwrnlcs, 29:861, 1962) he takes issue with
a previous paper by my colleagues and myself
(New Engl. 1. Med., 265: 101, 1961). In that
paper each of the arguments was based upon
LETTERS TO THE EDITOR 341 While Dr. Chamberlain apparently does not
like the words “some theoretical estimates” to
assess the quantity of edema fluid, even the
“theoretical estimate” was based upon the
measured skin water content in normal cliii-dren, as well as that in experimental animals, with the calculated differences based upon the
relative accumulation of fluid in the skin and
subcutaneous area during frank edema
(PEDI-ATRICS, 20: 105, 1957) as well as the specific
accumulation of fluid in tissues burned to
vary-ing degrees and by flame and scald techniques
in experimental animals (Fox & Lasker: Surg.
Gynec. Abst., 112:274, 1961; Fox & Baer,
Amer. I. P/zysiol., 151 : 1947). The statement
by Reiss et a!, (J.A.M.A., 152:1309, 1953)
re-garding the “copious losses” from the bum
sur-face cited by Dr. Chamberlain, was
subse-quentiy modified by Reiss et a!. in a later paper (I. Gun. Invest., 35:62, 1956) in which careful observations were substituted for previous
opinion. With relation to the reference by Cope & Moore (Ann. Surg., 126: 1010, 1957)
these authors carefully studied the increase of
thiocyanate space in five patients with
exten-sive third-degree burns, they equated the
ex-pansion of thiocyanate space with expansion of
the interstitial space due to burn trauma.
Al-though Cope and Moore believed the
expan-sion of the interstitial space was obligatory and
not the result of therapy ((Table IV) the
Corn-mentary in their paper referable to this
state-ment was: “It is of interest that the 8-litre
ex-pansion in extracellular fluid revealed by the
second measurement (five days post-burn) cor-related so closely with the difference between
intake and output during the first 48 hours,
8,937 ccs (Chart 1). In patients who are flooded
with water one cannot estimate the volume of
burn edema by the volume of fluid retained because the factor of renal function becomes so large, and a discrepancy between intake and
output may reflect renal damage.”
While it is always dangerous to extract a
single statement from a long and detailed
ac-count for fear of distorting the totality of the
information and concept provided, their
inter-pretation of that particular item was quite
ac-curate and is ai example of the great value of their paper. It is also consistent with the thesis
put forward in ours.
With relation to the urine output, the large
mass of evidence presented by Cope and
Moore, Evans and associates, Reiss et a!.,
Batchelor et a.l.-cited in our original paper-as well as the important data of Craber and Sevitt (I. Gun. Path., 12:25, 1959), as well as our own data, certainly strongly support the concept that urinary output does not reflect fluid input during the first 24 to 48 hours of
therapy. While one should be concerned when
the kidneys cannot cope with infusion of
cx-traordinary amounts of fluid by enhanced fluid
volume if one is to avoid pulmonary edema,
this does not preclude the concern we have
with the accumulation of fluid in the burned area. The data derived from our studies sug-gest that the extensive accumulation of fluid in the burn area is closely related to, and when
marked, dependent on, the administration of
excessive fluid. One might recall that Cope and
Moore pointed out that despite the huge
ex-pansion of the thiocyanate space with very large infusions of fluid or plasma, the variations in plasma volume were inconsequential. This
indicates that if hypovolemia did indeed exist,
apparently the huge fluid and plasma infusions
did not alter it; rather, most of the administered
fluid gravitated to the injured area.
The purpose of our paper was not to “take
away much while offering little of practical
value in return” but rather to set the record
straight by substituting a limited number of
observations for a large body of intense, but
somewhat misguided, opinion. No easy formula can do justice to generally precise fluid therapy for an individual patient. If one is given data
about how much fluid might be lost from the
burned area, what the limitations of renal re-sponse and urine volume are (supplemented by balance observations), clearly fluid therapy can readily be calculated by anyone with even limited knowledge of body fluid physiology. An example of this type of calculation was
in-corporated in the original paper in order to
“give something back . . .“ and in an endeavor
to offer something of “practical value . . .“
As far as being unable to do more than
present the facts derived from the observations, or to reduce them to a ridiculously simple ex-pression which would please all of the people all of the time, I plead guilty.
Actually, the Commentary was offered as an attempt to assess the contribution made by Dr.
Meeker and his colleagues with relation to
342 LETTERS TO THE EDITOR
paper. It was not an attempt to publish a
re-hash of our previous paper.
I suspect that Dr. John Chamberlain is
in-deed the spokesman for many less direct,
equally experienced, competent surgeons. If
the paper of my colleagues and myself was
provocative, I hope the provocation will lead to further studies to provide for extensive data which might be compressed into a simplified formulation. Until then, there is an old proverb
which states: “Equinus ad aquam offerri
pos-sibles est
Chicago 1 6, Illinois
J
ACE METCOFF, M.D.Michael Reese Hospital and Medical Center
Human Milk-Protein-Prematurity
To THE EDITOR:
Sometimes, in order to make an article brief,
authors quote others, but the interpretations of
the new authors may not reflect the context of the original observers. This has occurred in the quotation of several of our papers in a recent
article by Pincus et al.1
First we are quoted as agreeing “that small
infants where fed isocaloric diets gain weight
more rapidly on a diet having a higher protein content’ (author references 12 and 16). In reference 12,2 we state that infants fed 3.0 to
8.0 gm of protein per kilogram gained equally well. Only when the protein intake was below
2.0 gm/kg did the weight curve not rise as
well. Indeed, in this paper, we noted a few
babies taking more than 8 gm/kg protein who
gained very poorly. Reference 16 is an
ab-stract.3 In this abstract we note only that a
higher serum protein is found in those infants
fed a lower protein diet and do not mention weight gains. Unfortunately, the data on which this abstract is based were published in a not
easily available journal. Here we state “81
pre-mature infants have been fed formulas
provid-ing approximately 6.1 gm protein per
kilo-gram, and 81 similar infants, formulas
provid-ing approximately 2.5 gm protein per
kilo-gram. Both groups showed statistically equiva-lent weight gain, well-being, morbidity,
mor-tality, and total serum proteins.”
We are further quoted as agreeing “that
human milk provides sufficient protein for the needs of the premature.” As long-standing
ad-vocates of human milk feedings, we were
chagrined to find on the contrary that
un-fortified human 11111k did not support weight
gain in prematures as well as other feedings.
This was from very limited data in oIll\’ one of our weight groups. We, therefore, discontinued this type of feeding. Likewise we were unable
to relate protein intake to serum proteins. “There were no statistical differences in the serum protein values in infants who were fed 3 to 8 gm of protein/kg :‘day. In contrast, in-fants who were fed less protein (i.e., human
milk) have shown lowered serum protein
values.”2
We write this only because we too would
like to find the ideal feeding for premature in-fants and still feel that a high protein feeding may be harmful to premature infants.
REFERENCES
1. Pincus, J. B., et al.: Protein levels in serum of
premature infants fed diets varying in protein
concentrations. PEDIATRICS, 30 : 622, 1962. 2. Omans, W. B., et at.: Prolonged feeding studies
in premature infants. J. Pediat, 59:951, 1961.
3. Barness, L. A., et al.: Comparison of prematures
fed high and low protein diets. Amer. J. Dis.
Child., 94:480, 1957.
4. Comely, D. A., et at.: Comparison of prematures
fed with two different levels of protein. Pediat. Intern. (It.), 9:9-19, 1959.
WALTER B. OMANS, M .D.
LEwIs A. BARNESS, M.D.
CATHERINE S. ROSE, M.D.
PAUL Cy#{246}ncy, M.D.
Philadelphia, Pa.
EDITOR’S NOTE: Drs. Pincus and Gittleman
re-plied as follows.
To THE EDITOR:
In our article we referred to the publications of Barness et at. and Omans et a!. in three areas dealing with weight gain and with the effect of diets on serum protein levels. Barness
et at. in the American Journal of Diseases of
Children (94:480, 1957) state: “Rate of weight gain was slightly more rapid in infants fed the higher protein formula.” Again, Omans et at. in the Journal of Pediatrics (59: 955, 1961), state: “In the present study the babies who
were fed less than 2.5 gm/kg/day gained
poorly, while those who were fed 3 to 8 gm/ kg/day gained equally well.” These conclusions would lead one to believe that infants gain
better on diets higher in protein.
In the publication by Omans et a!. in the
