Bragstedt X 
THERMAL BURES 
Xi, H. Bragstedt, H. B. 
Professor of Surgery, University of Chicago 
I have been asked to discuss the modern treatment of "burns. 
It seems to me wise "before beginning with the treatment 
of burns to examine briefly what we know about the patho- 
genesis of burns, and the cause of death from burns. 
Previous to 1925 it was almost universally held that the 
cause of death from burns was the absorption of various 
toxic protein split products arising in the burned area 
as a result of the destruction of large amounts of tissue. 
About ten years ago that view gave way to the concept 
that death from burns was due to the large loss of plasma, 
from the circulating blood, with resultant decreased 
output of the heart, lowered blood pressure and general- 
ized tissue anoxia. Within recent years the concept 
has arisen that both factors may play a role in the 
cause of death in burns; that there may be an extensive 
loss of plasma from the vessels and in addition the 
absorption of poisons from the burned area.. The problem 
is still unsettled, and I should like to indicate briefly 
the evidence that we have, upon which we can base a 
tentative opinion. 
First, with respect to the pathology in burns, the local 
pathology varies all the way from the erythema of the 
first degree burn, the blistering and vesicle formation 
of the second degree burn, to the extensive eschar with 
destruction of the skin and the subcutaneous tissues in 
the third degree burn. It is important, I think, from 
the standpoint of treatment to realize that we cannot 
at the time of first seeing the burn make a sharp 
diagnosis or differentiation of the extent of the burn 
or determine the involvement of the deeper tissues. We 
cannot always distinguish between a second and a third 
degree burn. We know that the burn is of the third 
degree when subsequently we find that we have skin graft- 
ing to do. This is unfortunate, because if we know the 
extent of the burn at the time when it was first seen, 
more successful treatment might be devised. 
Perhaps the most important local change is the extensive 
edema in the burned area and the very large accumulation 
of plasma or plasma-like fluid in the subcutaneous 
tissues, and the very large loss of plasma through weeping 
from the burned surface. Besides this we may find 
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extensive charring or necrosis of the subcutaneous tissue 
also involving the muscles and even the bones in very 
severe burns. 
In addition to these local effects, certain systemic 
changes have been found to occur fairly constantly in 
severe burns. First I should like to call your attention 
to the changes which have been described in the liver. 
Areas of focal necrosis and fatty degeneration are not 
infrequently found. It is significant that some recent 
work has demonstrated ths.t tannic acid apulied locally 
or injected beneath the skin can produce focal necrosis 
and fatty infiltration in the liver, so that it may pos- 
sibly be that in some cases the focal necrosis and 
changes in the liver seen- in burns treated within the 
last 12 years may be due not to the burn but to the use 
of tannic acid. It is important, however, to realize 
that this change in the liver was described before the 
advent of tannic acid treatment, and has been found in 
burned patients who we re not given the tannic acid. 
The cause of this fatty necrosis and fatty change in 
the liver in burns in not entirely known. 
The kidneys in many cases are found to display acute 
glomerulitis, hemorrhage in the glomeruli and degenerative 
changes in the epithelium. The. gastrointestinal tract 
very often displays widespread hyperemia, superficial 
ulceration in some cases, and fairly deep penetrating 
ulceration in the duodenum occasionally in the pyloric 
part of the stomach or in the first part of the jejunum. 
This ulceration in the duodenum was first described by 
James Long in 1840 and subsequently by Curling in 1842 
and as you know is commonly called the Curling ulcer. 
The pathogenesis of this ulcer is unknown, but I might 
say to you that an attractive hypothesis suggested to 
account for it is based on some recent work of Wangensteen 
and his collaborators at the University of Minnesota. 
These men have found that the inplantation of histamine 
in beesi'/ax beneath the skin of experimental animals pro- 
duces long continued secretion of gastric juice by the 
stomach. This is due to the gradual liberation and 
absorption of histamine from the beeswax. Excessive 
secretion of gastric juice produces ulcers in the 
stomach or first part of the duodenum. There is some 
evidence that among the products which may be absorbed 
from a burned area is histamine and there have been a 
number of studies indicating that the level of the 
histamine in the blood in burns is slightly increased. 
It is conceivable then that the chronic absorption of 
histamine from the burned site may well provoke a con- 
tinuous secretion of gastric juice and the formation of 
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ulcers in the stomach or duodenum. This is, however, not 
a settled Question. I would like, however, to point out 
that it is difficult to account for the ulcer in the in- 
testines in turns on the basis simply of plasma loss. 
The adrenals often display hyperemia, and hemorrhage. The 
significance of this is not clear. We find similar hy- 
peremia and hemorrhage following intravenous administration 
of many types of tissue extracts' containing various 
protein split products. It is now felt, however, that 
the most significant abnormality in burns is the very • 
large loss of plasma, resulting in extensive hemoconcen- 
tration. The proportion of corpuscles to plasma rises from 
a normal of 44 or 45 per cent to as high as 65 or 70 per 
cent of the blood volume. There is thus a very large 
loss of the liquid part of the blood. A fall in the con- 
centration of chlorides in the blood has also been found. 
This was demonstrated first by Underhill and his associates 
a number of years ago. 
An increase in the clotting time of the blood also occurs, 
the mechanism of which is at present entirely obscure. 
It is not due to any alteration in the blood calcium, 
nor to any alteration in the fibrinogen of the blood or 
to its prothrombin content. A marked edema in the lungs 
and in the viscera has also been found. 
One view of the pathogenesis of burns holds that death is 
due to the escape of plasma from the vascular space 
through weeping from the burned surface, the SO' called white 
hemorrhage, accumulation of plasma in the subcutaneous 
tissue at the burned site, and escape of plasma through 
the capillaries in the lungs, liver and gastrointestinal 
tract. Realization of the importance of the loss of the 
liquid constituents of the blood in burns came about first 
through the work of Underhill and his associates in 1923. 
These men reported that a marked hemoconcentration occurred 
in burns, the hematocrit rising from the normal of 44 to 
as high as 65 or 75 per cent. A superficial burn in rab- 
bits on which their work was chiefly done involving one- 
sixth of the body surface caused a loss of 70 per cent 
of the total blood volume as subcutaneous edema. 
ITow it is important to know from the standpoint of treat- 
ment at least that this escape of plasma from the vascular 
space occurs with considerable rapidity. In tipping 
experiments where an animal was placed on a balanced table 
and a burn applied to one side of the body, accumulation 
of subcutaneous edema on the burned side of the body was 
manifested by tipping of the body toward the burned side, 
and this tipping was found to begin within a few minutes 
after the application of the burn. Others have found, 
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and we have confirmed this in our own experiments, that 
significant loss of plasma is well marked within 15 or 
20 minutes from the onset of the burn and may roach its 
maximum within four to six hours. 
It is important then for the physician to realize that 
in most cases a very marked loss of plasma from the 
vascular space has already occurred by the time the 
patient cones to the physician. We had the opportunity 
to take care of a patient in our clinic sometime ago whom 
we saw within 30 minutes after the receipt of the burns. 
The hematocrit was already above 50 and by the time the 
local treatment had been applied, which took 40 minutes, 
it rose to over 60, so that the striking rapidity of the 
loss of plasma, from the circulation is apparent. This 
is important to realize when we come to discuss the ra- 
tionale of the pressure treatment of burns. 
This large loss of plasma into the burned area with re- 
sultant decrease in the volume of the circulating blood 
brings about a fall in blood pressure and decreased cardiac 
output. The fall in blood pressure may go beyond that 
which can be compensated for by vasoconstriction, increase 
in the heart rate, the normal regulatory mechanism. 
There is some evidence that local tissue asphyxia re- 
sulting from long continued low blood pressure may produce 
a widespread capillary damage so that plasma escapes from 
the vessels not only in the burned area but also in dis- 
tant organs such as the lungs, liver, or gastrointestinal 
tract. 
This theory then attempts to account for the pathogenesis 
of burns not through the absorption of a toxic substance 
from the burned area, but from the loss of plasma from 
the vascualr spaces, primarily into the burned site as 
weeping from the surface and subcutaneous accumulation 
of plasma, and also to the escape of plasma into the lungs, 
gastrointestinal tract and visceral organs. 
The other point of view holds that death from burns is 
due to a toxemia due to poisons absorbed from the burned 
area which enter the circulation, produce widespread capil- 
lary damage and increased permeability, damage to the liver, 
kidneys, adrenal glands and gastrointestinal mucosa. 
There is now no dispute about the dangerous diminution in 
the blood volume and hemoconcentration in burns. The 
evidence upon which the intoxication theory of burns is 
based is non very firm. I am not going to analyze the 
earlier experiments in this connection, but refer to the 
work of Robertson find Boyd in 1923. These workers re- 
ported that extracts of burned skin and the blood of 
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■burned animals was toxic. These experiments, however, 
were repeated by Underhill and his associates, by Blalock, 
hy Harkins, and a number of others, and the results are 
contradictory. Some have reported increased toxicity, 
others no increase in toxicity, so that a final decision 
cannot be made at present. A significant contribution 
was made by Slkington and Roberts in 1940. These inves- 
tigators reported that patients \d.th severe burns may 
die even though the plasma loss and hemoconcentration 
present has been entirely corrected by the administration 
of plasma, indicating that some residuary defect exists 
even when the plasma that has been lost is replaced. I 
think this is a significant finding. 'I have no reason 
to doubt that the experiments indicating a slight increase 
in the amount of histamine in the blood are also valid. 
The significance of that finding, however, is difficult 
to assess. Whether there is sufficient liberation of 
histamine to produce a significant systemic effect is 
hard to say. The decreased coagulability of the blood 
however is a factor suggesting some systemic change. 
This decreased coagulability of the blood is apparently 
not due to the presence of some heparine-like substance 
in the blood. i 
I may state this experiment to you for what it is worth. 
We asked ourselves the question, is there absorbed from 
the burned area a sufficient amount of toxic material to 
seriously affect the animal? To get some data on this 
point we arranged for cross circulation between two 
animals, A and B, In this type of experiment where a 
large loss of plasma occurs in one of the animals, it 
is necessary to arrange for nuantitative cross circulation, 
otherwise the animal who is burned will receive all of 
the blood from the normal animal and the normal animal 
will bleed to death into the veins of the animal whose 
blood pressure falls. This was controlled by arranging 
for a quantitative cross circulation. When the cross 
circulation was established one of the animals of the 
pair was severely burned and continuous cross circula- 
tion was maintained beWeen the pair. The burned animal 
finally died at the end of four or five hours. The ex- 
periment was repeated a number of times. During the 
course of the burning the normal animal which was. re- 
ceiving the blood from the burned animal received as 
nuch as 3000 c.c., that is, all of the blood from the 
burned animal was circulated through the body of the 
normal animal four or five times. When the burned 
animal was moribund the animals were separated, and in 
each case we found that the animal which continuously 
received the blood from the burned animal survived, 
indicating that so far as one can Judge from this type 
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of experiment a sufficient amount of toxic material to 
cause death was not elaborated into the circulating 
blood. Offhand this sounds like a conclusive type of 
experiment. Tt has, however, certain limitations. If 
one, for instance, arranges for a similar cross circu- 
lation and then poisons one animal with such a substance 
as strychnine, giving animal A, let us say, a double 
lethal dose of strychnine, .wait for a minute or two for 
the strychnine to become distributed throughout the body, 
and then establishes cross circulation and maintains it 
continuously, the animal which has been poisoned with 
strychnine develops typical convulsions and goes on and 
dies, whereas the other animal which is constantly re- 
ceiving blood from the strychninized animal at the same 
time shows no signs whatever of strychnine poisoning. 
So we know that one of the characteristics of an active 
toxic substance is that it becomes rapidly fixed in the 
tissues and does not exist for any long period of time 
in the circulating blood. 
We may take it, I think, that when a burned animal or 
man dies he does not have more than a lethal dose of toxic 
material in his entire organism. The chances are good 
that most of that is fixed in the tissues and that very 
little of it is in the circulating blood. I point that 
out simply to indicate the very great difficulty of 
determining the presence or absence of a toxemai by 
examining the blood itself. 
I am unable to say now what the cause of death in burns 
is. My provisional feeling is that the most important 
factor responsible for the death of a burned patient 
within the first 24 to 48 hours is the large loss of 
plasma from the vascular space, I believe that it is 
the principal cause of death and for the symptoms that 
occur during the first 24 or 48 hours. I believe, how- 
ever, that it is probable that a certain amount of toxic 
material enters the circulation from the burned area, 
and that this toxic material produces widespread effects 
on distant organs, of which the ulcer in the gastrointestinal 
tract, the focal necrosis in the liver and diminished 
coagulability of the blood may be evidence. 
Now with respect to the treatment of burns. It seems to 
me that the principles involved in the treatment of burns 
are these: to relieve pain, replace the lost plasma, 
to restore kidney function, to protect the injured tissues, 
to prevent infection, to limit plasma loss, and to favor 
repair. 
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How, all are agreed that it is safe and useful to relieve 
the pain of turns by the use of morphine. The OCD recom- 
mends the administration of a hdlf grain*' of morphine and 
in our experience that has been satisfactory. Most writers 
caution against the use of a general anesthetic. A gen- 
eral anesthetic is unnecessary in adults, but I must 
confess in handling children I have felt that there was 
more advantage to the use of a general anesthetic than 
danger. However mostly we will have to do, I presume, 
with burns in adults, and I think pain can be adequately 
controlled by the administration of this relatively large 
amount of morphine. 
Second, replace the lost plasma. There is no debate 
whatever concerning the presence of marked heraoconcentra- 
tion in burns. All also recognize that very large amounts 
of plasma are necessary to restore the blood to its nor- 
mal state. There/is some disagreement concerning the 
wisdom of trying to replenish the lost plasma, immediately 
be a single transfusion if plasma is available, or whether 
it is not better to administer the plasma required in 
fractional doses. A large amount of plasma is required. 
A burn that involves 10 per cent of the body ordinarily 
will require a thousand c.c. of plasma, to restore the con- 
centration of blood to its normal level. I should like 
to point out, however, that the loss of plasma begins 
immediately after the receipt of the burn, becomes very 
marked within a few hours and continues for three or four 
days. Attempts have been made to devise a formula in- 
dicating the amount of plasma which ought to be given in 
an attempt to completely replace the loss of plasma by 
the time the patient is seen. I doubt that that is 
necessary. I think it is probably better to give the 
patient perhaps 500 c.c. of plasma when he is first seen, 
realizing that if the hematocrit is 70 that may bring the 
hematocrit down to only 65 or 60, then four or five or 
six hours later a second administration of plasma, re- 
peated again in five or six hours. I believe that is 
more beneficial than the administration of the entire 
volume of‘ 1500 or 2000 cc. when the patient is first seen. 
That large amount of plasraa is also often not available. 
The point I want to bring out is there is some experi- 
mental evidence indicating that the administration 
of the plasma and gradual correction of the hemoconcentra- 
tion has some advantage. 
Restoring kidney function. Many of these patients have 
a diminished urinary secretion or a complete anuria. 
That was evident in four patients that X saw a year or 
so ago. ¥e gave these patients a relatively large volume 
of physiological salt solution intravenously. I believe 
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one ought to give these patients as much physiological 
salt solution intravenously as one administers plasma. 
There is this objection to the administration of physio- 
logical salt solution: in the presence of damaged 
capillaries it passes rapidly into the subcutaneous 
tissue, and some authors have suggested that it not only 
passes out itself, but it carries plasma along with it. 
I doubt that, however* It does pass into the subcutaneous 
tissue and to a certain extent increases the edema, but 
it is very effective in restoring urinary flow, and in 
view of the evidence that we have, not good to be sure, 
but suggestive evidence, that a toxemia of some type may 
exist, I believe it is \vrise to correct the anuria that 
exists in severe burns, even at the risk of increasing 
the local edema. 
In burns there is always more or less hemolysis of the 
blood, destruction of corpuscles resulting in staining 
of the plasma with hemoglobin. Whether this is due to 
the destruction of the corpuscles locally by the heat 
or whether it is due to a toxemia is not known, but a 
moderate degree of anemia may be looked for in severe 
burns, even if infection is avoided, and particularly 
so if infection occurs. So that blood transfusion is 
almost always indicated in severe burns. 
Now, the local treatment of burns. The efforts here are 
to protect the injured tissues, to prevent infection, 
to limit plasma loss, and to favor repair. All are 
agreed that the prevention of infection is the most im- 
portant single factor in the local treatment of burns. 
The organisms that are commonly present in the skin are 
usually not serious. The serious organisms that infect 
burns are usually deposited there from the nose and 
throat of the physician or attendant who first sees the 
burn. This means that the man who takes care of the burn 
must exercise the same aseptic precautions that he 
exercises in a laparotomy; i.e., rubber gloves, mask, 
gown, and sterile technique. If a burn is seen shortly 
after it is received, it is likely that the burned area 
is sterile. If it has not been contaminated by organisms 
from the nose and throat of the patient or from the first 
aid attendants, it is likely that it could be success- 
fully handled without any attempt to clean the wound. 
It is interesting to note, in the Cocoanut drove disaster, 
results in some of the patients brought to the Massachu- 
setts General Hospital. Here the wounds were sinroly 
covered with sterile dressing when the patients were first 
received and then a bland mild antiseptic ointment and 
a pressure dressing were applied. This sufficed to pre- 
vent any serious infection in a large number of the 
h- 1507-P15-N0BU* COS-WP Dragstedt X 
patients so treated. 
If the burn however is dirty, the tissues are covered 
with oil or dirt or foreign bodies, I believe it is 
wise to adopt the technique recommended by Sumner 
Koch of Chicago, that is, careful cleansing of the wound 
with sterile water and soap, generally be means of cotton 
pledgets. He has demonstrated that it is possible to 
mechanically convert an infected wound into a sterile 
wound by washing with soap and water. It is probably 
wise also to remove the dead skin around blisters and 
cut away all dead or devitalized tissues. 
Now, we come to a question about which there is a dif- 
ference of opinion. In 1925, S. C, Davidson, introduced 
the tannic acid treatment of burns, and there can be no 
question that this was at the time of a great advance. 
At this period the significance of the loss of ■plasma 
in the pathogenesis of burns was not fully appreciated. 
The application of tannic acid limits the local loss of 
plasma, because it provides a tough tanned membrane 
which stops weeping and provides a certain amount of local 
compression. The rational of the tannic acid treatment 
as introduced by Davidson vas curiously enough that the 
tannic acid by tanning the burned area limits the ab- 
sorption of poisons. That was the theory back of the 
treatment. 
Irrespective of that, it must be conceded that the 
introduction of the tannic acid treatment of burns saved 
a great many lives. Why then do people object to the 
tannic acid treatment of burns at the present time? 
The objections are based largely on these points: 
With the recognition of the significance of the loss of 
plasma and the availability of plasma for infusion, the 
necessity of using tannic acid for that purpose is not 
so important as it was at first. 
Second, it is altogether probable that tannic acid des- 
troys a certain amount of surviving epithelium in a burned 
area. It coagulates not only dead protein, but it 
destroys many islands of surviving epithelium in the 
depths of hair follicles from which island regenerating 
skin might otherwise cover the burned site. 
I have no doubt from my own experience that tannic acid 
often converts a second degree burn into a third degree 
burn. Of greater significance, hox;ever, is the point that 
the tannic acid coagulum over a. burned area handicaps the 
surgeon in the treatment of infection. It is likely that 
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if one could "be sure that all burns were aseptic or could, 
be made so, most of the objection to the tannic acid 
treatment would, vanish, but in my experience this does 
not obtain. In very large burns, in spite of a reasonably 
rigorous attempt to wash the wound, clean, and a certain 
amoung of judgment has to be exhibited here for fear of 
damaging the tissue, a variable number of organisms per- 
sist. If a dense coagulum is completely over the burned 
area, the presence of an early infection is difficult 
to detect, pus may accumulate beneath the membrane and 
a large part of the wound may become seriously infected 
before it is realized. 
That is the first objection that I have to the tannic 
acid treatment. 
Another point comes in the demonstration of the toxic 
effect of tannic acid on the liver. There seems no 
doubt that tannic acid itself can produce focal necrosis 
and fatty degeneration of the liver. Whether this happens 
in any large number of burn cases treated with tannic 
acid is not possible to say, but I believe that, it is a 
point that ought to be kept in mind. 
An alternative is illustrated by a method of treatment 
popularized by Sumner Koch and Allen and reported in 1942. 
With a large series of burns Koch and Allen demonstrated 
that it was possible to secure comparatively aseptic 
wounds by washing with sterile water and soap, with an 
asentic technique. 
After the wound is cleansed, vaseline gauze and a protec- 
tive dressing is immediately applied and a pressure 
dressing. This is done with the aid of sponges, with 
gauze, with the amplication of a roller or an elastic 
bandage, 
The thought behind the pressure dressing is that the pres- 
sure dressing limits the. continued escape of plasma from 
the burned area., by the application of mechanical pressure. 
It also immobilizes the limb and the injured joints quite 
effectively, almost as effectively as a, plaster cast, 
and contributes thereby greatly to the comfort of the patient. 
We have used this method of Koch and Allen, and decided 
that it represents a real advance. We have added to it 
one point. Instead of using vaseline gauze as a protective 
dressing we have made use of the specific bacteriostatic 
action of the sulfonamides. The sulfonamide that we have 
preferred is sulfathiazole, because it is more versatile 
in its action against organisms than the other sulfonamides, 
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and it also seems to have an analgesic action. 
Dr. J, Garrett Allen of clinic prepared sulfathiazole 
20 per cent in an ointment base, and we have used this 
on gauze, in place of the vaseline of the Koch and Allen 
pressure dressing method. 
I believe this represents the best method of treatment 
of burns at the present time; debridement, cleansing, 
the application of an ointment protective dressing, 
which may well be one of the sulfonamides, and the 
pressure dressing. 
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