H. C. (Horatio C.) Wood.

Thermic fever; or, Sunstroke online

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ring sooner when the fluid is allowed to coagu-
late spontaneously. When the acid forms it alters
very materially the color of the liquid, and by set-
ting the latter aside in a glass vessel in a cool room
he was enabled to watch the change into a deep
reddish-brown liquid, occurring in from twelve to
twenty-four hours, whilst not a trace of turbidity
existed. This change of color I myself have noted
as occurring just before coagulation, and think
therefore that Morgan (loc. cit, p. 329) is mistaken
when he says the coagulation of the muscle fibrin
precedes this acidity; a mistake which might very
well have been a mere slip in the manuscript, and
it is well known he did not live to read the proof
In a second paper in the Sitzungsber. der k. bay.
Akad. d. Wissensch., i860, entitled "Untersuch-
ungen fiber die Muskelstarre," Harless attempts to
establish the theory that although coagulation of
the myosin and post-mortem rigidity occur at the
same temperature and consentaneously, the latter
is not due to the former, but to a physical action
of the acid developed upon the muscular fibrillae,
shrinking them up. I do not think, however, he
succeeds in establishing this, and believe that it is
disproven by the facts that in some muscles the
acidity does not develop (see Morgan, loc. cit., p.


329), and that washing the acid out of a muscle by
an alkaline solution will not restore its contractility
when rigidity has fully set in. There can be no
doubt, however, of the close connection between
the acidity and the coagulation of the myosin.
A circumstance illustrating this, mentioned by
Morgan (loc. cit, p. 333), is the action of a ten per
cent, solution of common salt on a rigid muscle.
This dissolves out the myosin, and leaves the
muscle limp and translucent, and at the same time
free from acid reaction.

The only objection to the coagulation theory
worthy of notice is found in the circumstance that
muscle which has become rigid after the cutting
off of the circulation from it, can be made to regain
its pliability and contractility by removal of the
arterial ligature, or that muscle which has become
rigid after the death of the animal can be restored
by the injection of warm blood. As early as 1834,
Dr. Jno. P. Kay (Treatise on Asphyxia, p. 143)
noted that if the circulation was arrested in a limb,
the muscles soon lost their power of contracting
under the influence of galvanism, but recovered it
when the obstruction to the passage of the blood
was removed.

His experiments have been repeated and ampli-
fied by various observers, especially by Brown-
Sequard (Comptes Rendus, June, 1851) and Prof
Stannius, of Rostock (Archiv fiir phys. Heilkunde,


1852). The experiments of the first of these ob-
servers were made both on man and animals; the
details it is needless here to speak of, but the results
arrived at were, that cadaveric rigidity in animals
could be overcome after it had lasted from ten to
twenty minutes, and in man a muscle which had
been rigid for nearly two hours could be restored.
I have not seen the original account of Prof Stan-
nius's experiments, but, as quoted, they are very
similar to those of Brown-Sequard,and the results
arrived at only differ in so far that Stannius suc-
ceeded in restoring the hind legs of a puppy which
had been stiff" and cold for one hour. It is this
possibility of restoration which has been urged as
an objection to the plasmic theory. As stated by
Kiihne, however, it does not seem to be a fatal ob-
jection. The first coagulation of the muscle plasma
does not necessarily imply the immediate death of
the fibre. And it is conceivable that while in a
condition of partial coagulation, as it were, the
plasma might yield to the solvent powers of the
warm alkaline blood and the renewed activity of
the surrounding life forces, and be brought into
such a state as to be removed, especially as it has
been shown that the myosin can be washed out
and the muscle rendered limp by a strong solution
of salt. In Brown-Sequard's experiments it wis
found that the blood changed its color from arte-
rial to venous during its passage through the arm,


showing that vital action was recommenced. Fur-
ther, it is implied by the experiments both of Brown-
Sequard and Stannius, and definitely proven by
those of Kiihne (loc. cit.), that there does come a
time when the rigid muscle cannot be restored,
although through the unbound artery the blood
courses into the capillaries and veins with steady,
free, persistent current. If the contraction were a
vital phenomenon, this could not be, because the
muscle should relax as soon as dead, and, not
being dead until relaxed, whilst still rigid ought to
be capable of restoration. In this view, then, the
assumed objection is rather a confirmation than a
valid objection to the plasmic theory.

This being so, I feel forced to accord assent to
the proposition, that thermic and post-mortem rigid-
ity are alike due to the coagulation of a plasma in the

This proposition being acceded, the question
naturally presents itself. Is death in sunstroke due
to the coagulation of the plasma by heat?

It is evident that in determining this question at
least two lines of approach are open, — the one,
that of absolute ocular and palpable examination,
determining whether or not the heart does stop
before respiration, and whether the muscles are
absolutely dead before general death; the other,
the comparative studyof the temperatures at which


coagulation of myosin occurs, and of the death
temperature in fatal heat or sunstroke.

Along the last of these roads I shall first ap-
proach. Vallin (loc. cit., p. 143) believes that co-
agulation of the myosin is the cause of death.
He says, — after detailing the fact that muscles
always become rigid at 45° C. (113° F.), — "The
death has always taken place at the precise mo-
ment that the temperature of the blood attains 45°
C, and a thermometer introduced into the cavity
of the heart did not vary more than some tenths
of a degree above or below this point; so that it
affords, as it were, a sort of natural realization of
the coagulation of a muscle by plunging it into
water at 45° C. The diaphragm, after the heart,
is the muscle which becomes rigid the most quickly,
and all the world acknowledges, after Claude Ber-
nard, that the point of greatest heat in the body is
where the vena cava traverses the diaphragm. It
is easy, then, to understand why at death the heart
and diaphragm are rigid, whilst the muscles of the
trunk preserve their contractility. Coagulation com-
mences with the left ventricle, which becomes rigid
and immovable; its cavity is effaced, and hence is
explained the relative arterial anaemia which all the
organs present. The right ventricle becomes rigid
more slowly and irregularly, and preserves in some
cases for a time its activity, so that the blood of
the pulmonary circulation, not finding access to


the left ventricle, accumulates in the lungs, pro-
ducing an enormous congestion, and sometimes
rupture. Further, the inertia, or, to speak more
accurately, the rigidity, of the diaphragm interferes
with the respiration, and adds the effects of asphyxia
to those produced by stoppage of the heart."

The temperature at which myosin coagulates
has already been shown to vary, but to be in warm-
blooded animals often above 45" C. or 113° F.
The testimony of Vallin, that the death tempera-
ture agrees with this, has just been cited, and in
another place in his memoir (p, 139) he says the
temperature at the moment of death varies from
44° C. to 46.1° C. Claude Bernard states that the
death temperature ranges from 43" C. (109!° F.)
to 45° C. (113° F.). Dr. Stiles says the tempera-
ture never rose above 115" F., and was often one
or two degrees below it.

The testimony of Vallin must be received with
some guardedness, as he is so fully committed to the
support of a theory. It will be seen that the experi-
ments of both the other authorities indicate that
whilst in some cases 113" F. is attained, in many
others the death temperature is much below it.
My own experiments, already detailed, confirm
this testimony, the rectal temperature at death
varying from in" to 114° F.

Dr. T. Lauder Brunton, in experiments reported
in St. Bartholomew's Hospital Reports, vol. vii.,


states that the upper limit at which the heart, when
heated, stands still varies in different cases, but
that in the stronger animals it is between 1 13° and
1 14" F., and even above. He has seen the heart,
however, beating actively at 115" F., and still under
the influence of the vagus nerve. These tempera-
tures, however, he remarks, were taken in the
rectum, whilst the arrangement of the heating
apparatus was such that the probabilities are the
temperature was somewhat less in the thorax than
in the abdomen. His results, I think, are further
vitiated by the fact that the animals were all nar-
cotized either with chloral or opium. In pigeons
the fatal temperature was always up to 120° in my
experiments; but there can be no doubt that the
coagulation point of myosin in these birds is higher
than in mammals, as their normal temperature is so
much higher. They must therefoj'e be left out of
consideration in discussing the question in regard
to mammals.

From these different views of the subject it may
be safely inferred that in some cases where an
animal is killed by overheating, the temperature
reached during life is that at which myosin removed
from the body coagulates, but in others it is a de-
gree or two below the point.

Further, it seems very probable that the myosin
influenced by life forces, and by the steady alkaline
current of the blood, would resist a heat in living


muscle which would coagulate it instantly under
other conditions. Confirmatory is the statement
of Dr. Brunton, already cited, that he has seen the
heart beating fairly and still under the influence of
the vagus when the thermometer in the rectum in-
dicated 115° F.

Looking at the question under consideration
solely from this point of view, the answer is some-
what doubtful, but appears to be that in some cases
it is very possible that death of the animal may be
due to direct coagulation of the cardiac myosin
by heat, whilst in other cases it is most improbable.

It is very possible that the mode of applying the
external heat, and e.specially the intensity of the
latter, may affect the result. Certainly my own ex-
perience is much opposed to the idea that a bodily
temperature of 115° F. is often attained in killing
cats and rabbits by heat.

The second means of deciding the question leads
in a more positive manner to a definite conclusion.
My own experiments were carefully made with a
view of determining the matter, and were very uni-
form in the result.

In no case that was closely studied did the heart
cease to beat before arrest of respiration. In Ex-
periment I the heart beat very feebly and imper-
fectly after the opening of the cadaver; in Experi-
ment 2 the animal may have been dead fifteen
minutes before the autopsy. In Experiment 3 the



heart was found beating quite actively after death,
and was seen to become suddenly rigid. In Ex-
periments 4,. 5, and 6, on pigeons, the pulsations
of the heart could be felt continuing after the cessa-
tion of respiration. In Experiment 7 the thorax
was opened and the regular beat of the heart
ocularly demonstrated after respiration had ceased.
In Experiment 8 death took place from a centric
convulsion, and the heart went on for some ten
minutes with a strong, vigorous beat.

Further, if it be true that an animal dies from
coagulation of the myosin of the heart, it is very
apparent that if, by any artificial means, it can be
cooled before such coagulation has occurred, whilst
the heart is still beating, recovery must result, or
at least death be averted for the time.

That an animal may, however, be cooled down
to its normal temperature, whilst the heart is beat-
ing, and yet the fatal result be in no very perceptible
degree postponed, is shown by the following experi-
ment :

Experiment 12. — Pigeon put in hot box at 1.53 p.m.
Temperature, 114°. At 2.14 the temperature was 117°. The
pigeon was now taken out of the box very ill, unable to
stand, but with the heart beating regularly. It was plunged
into cold water, and the temperature reduced to 105°. It
did not, however, revive any, and died in some ten minutes.

The results of my experiments viewed alone are,
then, very positive, that death does not generally


occur from coagulation of the cardiac myosin, but
from arrest of respiration.

Claude Bernard (loc. cit, p. 134), on the other
hand, says, " It appears still very possible, at least
probable, that there is a coagulation of the myosin,
and that this is the cause of the death of the mus-
cles, and of the heart in particular! The manner
in which heat causes death is, then, perfectly ex-
plained. However, as the animals can be taken
from the stove a few moments before the fatal issue
and not die for many hours, or even for many days,
it seems necessary to admit that there are many
other grave alterations produced by the heat."

Modifying my own results by those of Claude
Bernard and Vallin, I think the following proposi-'
tion expresses the truth :

Death in the lower animals from sunstroke or
heat fever, not produced by a sudden intense heat,
occasionally is the result of coagulation of the
cardiac myosin ; but in many instances, and prob-
ably in the majority of cases, is not so produced,
but is the result of arrest of respiration.

If it be true that when an animal is kept in the
intensely heated atmosphere until death, it suc-
cumbs often from other causes than the coagulation
of the muscular plasma of the heart, it would seem
that much more frequently would man suffer and
die from these other causes. His nervous syste'm,


especially the cephalic, is so much more susceptible
that it would be expected to suffer more than that
of the animal. More than this, in the experiments
I have detailed, the external heat is steadily kept
up until death, and hence the body of the animal
attains the maximum temperature. Not so with
man ; very generally the external heat is removed,
but death takes place nevertheless.

It is necessary, therefore, to study the effects of
heat on man separately from that on animals, to
determine whether death does result from coagula-
tion of the myosin of the heart ; and I shall ap-
proach the subject as before.

First, thenj what temperature is attained in cases
of insolation or coup de soleilf

Unfortunately, very few close clinical records
have been kept which can throw light on this point.
In India, especially, the suddenness and epidemic
nature of the affection, the fact that it mostly occurs
during the most laborious and trying periods of
campaigns and marches, and the circumstance that
the doctor is himself generally on the border of an
attack, all combine to prevent any clinical work
beyond what is necessary for the safety of the

The following table, taken from Dr. Levick's paper
in the Pennsylvania Hospital Reports for 1868,
represents, however, sufficiently the disease as it
occurs in the United States:







Tt'ittfi. Max. observed.*


New Orleans.


113° F.








104° after death.




110° after death.
























112° after death.



H. C. Wood, Jr





108° after death.















I09°-iio° after death.

An examination of this table will show that in
no case was a temperature anywhere near 115° F.
reached, either before or after death ; and that in
the large majority of cases the highest point at-
tained was not within six degrees of that degree;
although it is very probable that the temperature
given does not always represent the actual maxi-
mum, yet the evidence seems irresistible that in the
majority of cases of insolation in man the bodily
heat does not become sufficient to coagulate the
cardiac myosin. The results of observation are in
close concord with this conclusion. Earlier in this

* Proof seems wanting that the temperatures noted were actually
the highest attained in all cases.



paper I discussed the modes of death in sunstroke,
and it was, I think, clearly proven that in the gen-
erah'ty of cases death is immediately produced by
a failure of respiration, or by a gradual consenta-
neous failure of respiration and circulation.

The conclusion seems to follow inevitably that
in the ordinary forms of human sunstroke death is
not due to the coagulation of the cardiac myosin,
and that the latter change and consequent hard-
ening of the heart is a post-mortem phenomenon,
occurring directly after death.

In the discussion of the clinical history of sun-
stroke, it was stated that there is a distinct class of
cases in which syncopal death occurs suddenly.
A study of these cases is evidently here in order.

It is a fact well known to sportsmen that rigor
mortis comes on with extraordinary rapidity after
severe muscular exertion. A rabbit or hare which
has been run for several miles by a dog will, on
being shot, perhaps, roll over once or twice and
be picked up perfectly stiff The same thing has
been observed in the tetanus produced by strychnia,
the spasmodic muscles being said to sometimes
become rigid even without relaxation. Qf these
facts there can be no doubt, as they are testified to
by every investigator. (See Hermann, Grundriss
der Physiologie des Menschen, Berlin, 1870, p. 228.)

The explanation of this, if the theory of post-
mortem rigidity herein advocated be correct, is


that the myosin under such circumstances under-
goes some peculiar change by which its tendency
to coagulation is increased.

Dr. Harless (loc. ctt.) has experimentally proven
this to be the case, for he found that myosin pre-
pared from a rabbit tetanized with strychnia coagu-
lated at 42" C. (lOjf ° F.), whilst that from a similar
non-tetanized rabbit did not change until 48° C.
(ii8|° F.) was reached.

Certain experiments which I have performed
would seem to illustrate this fact by its opposite.
In Morgan's work (loc. cit., p. 332), the following
method of preparing myosin in large quantities is
given : " Enough common salt in powder is mixed
with snow in a cold vessel to form, when thawed, a
one per cent, solution, and this mixture rubbed up
intimately with one-fourth of its weight of shavings
of frozen frog's muscle is, while still at 3° C,
thrown on a piece of linen ; then the liquid is
filtered several times through paper wet with a
cold one per cent, solution of common salt set in a
cold glass funnel, and each time the filter clogs
a new one is substituted for it."

I followed this process, but not so closely, per-
haps, as I ought, straining only through the linen,
and perhaps having the salt in excess ; and got a
thick, syrupy liquid, which did not undergo distinct
instantaneous coagulation at a lower temperature
than 1 13° F. The frogs I used were frozen almost



stiff, and had been absolutely torpid for months,
and to this circumstance I attribute the slight tend-
ency of the myosin to coagulate, so that the propo-
sition may be stated that long rest of a muscle
diininishes the tendency of myosin to coagulate.

It is very plain a priori that these facts must be
true of man, if of animals; and clinical observation
certainly confirms them.

As a proof of this it is only necessary to refer
to a paper on " Instantaneous Rigor as the Ac-
companiment of Sudden and Violent Death," by
Dr. Jno. H. Brinton, in the American Joui:nal of
Medical Sciences, 1870, p. 1870. In this exceed-
ingly interesting memoir the sudden occurrence of
such instantaneous rigor is very clearly proven by
the testimony of the author and other eye-witnesses
as being frequently seen on battle-fields. Under no
circumstances is the excitement more intense, or
the muscular system more strained, than on the
field of battle ; so that the evidence is certainly
complete that both in man and animals excessive
exertion predisposes to coagulation of myosin,
and renders it liable to alter at a temperature
decidedly below the normal point of change.

The cardiac variety of sunstroke is said by the
Indian authorities to occur especially in action,
rarely during marches, never in barracks. As an
example of it may be cited the account given by a
witness to Dr. Parkes, and incorporated in his work


on Hygiene (Pract. Hygiene, 2d edit., p. 360), of
an occurrence during the first Chinese war. The
98th Regiment was marching on a very hot day,
and the surgeon who was with the rear-guard
stated to Dr. Parkes that the men fell suddenly
on their faces, as though struck with lightning,
and, on running up and turning them over, many
of them were already dead. Dr. Maclean, who
was present at this occurrence, confirms the ac-
count given by Dr. Parkes, but states that it was
at the attack on Chian-Kiang-Foo. The men
were thickly clothed, with tight accoutrements and
tight, rigid stocks, and were charging up a very
steep hill. A great number of them were stricken
down, and fifteen died instantly, falling on their
faces, and giving merely a few convulsive gasps.

The points worthy of note in this history are, —
first, that the men were making violent exercise
going up-hill, so that the heart must have been in
exceedingly active exertion, increased by the im-
pediment to the circulation afforded by the tight
accoutrements ; second, that the attacks were in-
stantaneous and syncopal in their character. To
my mind the conclusion is irresistible that death
was produced by sudden coagulation of the myosin
of the cardiac muscle, and consequent rigid arrest
of the heart's action.

Vallin seems to think that the arrest of respira-
tion, when it occurs before or simultaneously with



the cessation of the heart-beat, is due to a coagu-
lation of the myosin of the diaphragm. I think,
however, that the disproof of this, except as a mere
possible rarity, is so plainly contained in what has
been said about the heart, that it is not necessary to
dwell upon it. I will merely refer to Experiment
10, in which, although the cat died of sudden arrest
of respiration, the diaphragm distinctly reacted to
the stimulus of galvanism fifteen minutes after
death, and also to the fact that is shown in my
clinical I'ecords, that in man general muscular rigid-
ity is often not developed within the first hour after
death from insolation.

The prolonged study of the muscular system in
insolation has, then, produced the following conclu-
sions :

1st. Excessive rigidity of heart, due to a coagu-
lation of its myosin, is a very pathognom^onic lesion
of sunstroke.

2d. That in most cases it is a post-mortem, rather
than an ante-mortem, phenomenon, occurring di-
rectly after death.

3d. In certain cases, the so-called cardiac variety
of sunstroke, death is probably due to a sudden
ante-mortem coagulation of the cardiac myosin,
and consequent instantaneous arrest of the heart's

4th. That the muscles after death from heat
fever very soon become rigid, sometimes do so


instantly, and that such rigidity is of the same
nature as ordinary post-mortem rigidity.

5th. That while it is conceivably possible that
death from asphyxia may occur from coagulation of
the myosin of the diaphragm and other respiratory
muscles, it is exceedingly probable that in man
death never does actually occur from such cause.

Nervous System. — Having completed the study
of the action of heat upon the muscles and their
pathology, so to speak, in sunstroke, it seems next
in order to take up the nervous system. To any
one who has witnessed a case of coup de soleil, the

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Online LibraryH. C. (Horatio C.) WoodThermic fever; or, Sunstroke → online text (page 4 of 10)