Val. 3

THE EARLY RECOGNITION AND TREATMENT OF SHOCK *

Cranes R. Drew, MLD., Med. D.Se.t
Waskington, D. C.

Ix 1745 LeDran (1) described traumatic shock as a state in which there
_is arterial spasm, capillary stagnation and circulatory insufficiency.

I should like to start with these observations and present a simple
coneept which seems to offer a workable approach to the better under-
standing of the mechanism of shock. Next, I should like to demonstrate
a series of tests which have proved of value not only in rapidly assessing
changes in the peripheral circulatory system but also, at times, in pre-
dicting the onset of shock. Finally, I should like to suggest a method of
treatment based on this concept and data from several cases in which
treatment was guided by these tests.

In 1923 Gustav Ricker (2) published in book form a series of studies
relative to the effect of irritative processes on the terminal arterial seg-
ment. This segment, consisting of a small artery, arteriole and capil-
lary tree, he considered the fanctioning unit of the peripheral vascular
system, and compared it to the axon, the basic unit in the nervous sys-
tem, or the nephron, the functioning unit in the urinary system. He
stressed the segmental nature of this terminal unit and pointed out the
different effects on the arterioles, venules and capillaries, as a result of
different degrees of stimulation or irritation. To me, it seems, there is
no real difference hetween a stimulus and an irritant except that the
latter is a stimulus which acts too strongly over a short period of time -
or when of moderate intensity is continued too long, thereby transcend-
ing physiological limits.

Professor Horst Oertel (3) of McGill University, to whom I am in-
debted for this approach to the better understanding of a diffieult prob-
lem, in carrying on and amplifying the experimental work related to
Ricker’s concept of inflammation has demonstrated five rather distinct
phases in the changes which take place in the peripheral vascular seg-
ment under varying degrees of irritation. They are:

1. Iscurnma

Under sudden but unsustained lecal irritation, such as that produced
by a sharp crack with a switch on the skin, strong vasoconstriction is ap-
parent in each of the terminal segments. Blood flow ceases and the part

Seen een ee ee eae ee en en nen
York, N. ¥.

ork; From the Department of Surgical Pathology of Columbin University, College of
eiana sed Burgeo’ tha Department ot Sergery of the Prosbylerian Hoogital is New eek GAY
and the Department of Surgery of Howard. University in Washington, D. C.
’ 3%6
Mer, 1942 Eanty Recocxrniox axp Treatuent or Suock 177

becomes blanched. Local injury of capillaries will set up not only a
reactive hyperemia when the irritant is removed, but throngh reflex
nervous impulses or chemical changes thought to be of the “‘triple re-
sponse”’ nature as described by Lewis (4), inflammatory changes will be
seen to follow in the surrounding tissue. ‘With an irritant of this type
there is little systemie reaction for the damage done is usually slight.
Such slight injury does not cause shock.

2, Hyrenesa

On the other hand, under mild but prolonged irritation there may be
an incipient and transitory vasoconstriction of the whole segment, bat
the sustained response is that of generalized vasodilation in a manner
quite similar to that observed following slight nutritive over-activity of
a part or of an organ. Such a state may be seen following a moderate
degree of “‘sunburn.’* Such a mild irritant, acting for a longer period
of time over a much wider area, may have definite systemic effects.
There is a definite transndate as a result of the capillary ectasy with
upset in water and mineral balance. The cardinal symptoms and signs
of inflammation are present and may be explained by the observable
phenomena in the peripheral vaseular tree. Yet because an irritant of:
this type is mild, complete restitution to anatomical and functional in-
tegrity is the usual finding.

3. Pentsratic Puase

Under persistent, stronger irritation there is at first a transitory

- ischemia, then a period of diminished constrictor irritability, the arteri-

oles and capillaries are dilated, transudation takes place for a while but

later exudation is marked. The extruded fluid not only tends to di-

minish effective circulatory volume by virtue of lost fluids but also up-
sets osmotic balance.

The condition of the peripheral vascular unit seen in this peristatic
phase of localized inflammation is observed over a wide area only when
there is excessive central stimulation with resultant inhibition of the
vasoconstrictive center. Goltz (5), as early as 1863, suggested that any
excessive psychic stimuli such as fright, somatic stimuli such as pain, or
excessive stimulation along afferent nerves such as caused by a blow to
carotid sinus or celiac’ plexus, may cause inhibition of the vasomotor
center and consequent generalized vasodilation, pooling of blood in the
periphery and fall of blood pressure. This is the state of a patient in
so-called primary shock. This is not the subject under discussion at the
moment, but it is of great interest to anesthetists for this is exactly the
state of affairs found following spinal anesthesia. Anesthetists have
learned to prevent the onset of this type of shock incident to spinal anes-

_thesia by preoperative therapy designed to counteract the vasodilatation
without affecting the anesthesia. Gesell (6) long ago showed that ani-
178 Cuantes R. Drew

mals might survive with very low pressures following spinal seetion,
whereas animals with much higher pressures went rapidly down hill
when they were in secondary or surgical shock. In the inflammatory
process the peristatic phase is a brief one. So is primary shock a
transitory state, for the patient either recovers with restoration of
vasomotor tone or the condition passes into a state of true surgical shock. ©

4, Pnesratic Puase

Under stronger irritation, be it in the form of trauma, bacterial
toxins, heat, cold, electricity, nerve impulses, or hormones, there is a
tendency for the whole segment again to be constricted, but soon the
capillaries begin to tire and dilate while the arterioles and venules, being
more heavily museled and not so readily fatigued, remain somewhat
constricted. Circulation is slowed, blood begins to pool at the pe-
riphery, cyanosis appears, hemoconcentration begins,.and circulatory
volume begins to decrease. :

This is the stage observed in the early stages of surgical shock. This
is the phase which must be recognized and must be treated. The blood
pressure may remain surprisingly normal for a long period after these
changes have begun. All of the compensatory mechanisms are brought
into play. .

If the irritant is even stronger and more persistent, the arterioles are
seen to constrict even more tightly, blood flow is more markedly de-
creased, white cell diapedesis begins early, and gradually there is com-
plete paralysis of the capillary bed, with loss of red cells into the inter-
stitial tissue, that is, a hemorrhagic exudate. This is the picture seen in
severe infections, in severe anoxia such as may occur in an obstrueted ”
loop of the bowel, or in profound shock.

The blood becomes more viscid with loss of fluid, the rate of flow is
diminished, the pulse becomes more rapid with incomplete filling of the
heart, the venous pressure disappears and the signs of tissue anoxemia
begin to appear. It is this fourth or prestatic phase with which we are
coneerned when considering surgical shock. It is imperati¢e that this
state of the peripheral vascular system be ascertained before collapse is
complete. This arteriolar vasoconstriction must be released, capillary
tone must be restored, and fluids must be returned to circulation before
the changes become irreversible.

5. Static Prase

Finally with extreme or markedly prolonged irritation both the ar-
terioles and venules as well as the capillaries will be seen to be widely
dilated, with cessation of peripheral blood movement and ceasation of
all exudation. Preterminally small arteries will still be seen to be ca-
pable of responding and the resulting spasm may result in almost com-
plete occlusion of the lumen. Here the precipitant drop in blood pres-
sure is seen; anoxia resulting from the inadequate blood supply ex-
Eanty Recocxtriow ayp Treatwext or Sock 179

presses itself in the skin by cold, dusky cyanosis, in ‘the lange by rapid
and shallow respiration, in the muscles by great the kidney
by anuria and in the building of waste products of metabolism in the
blood stream, in the brain by apathy or coma and, finally, death ensues
as all tissue respiration ceases.

I shall make no attempt to settle the question of the etiology and
mechanism of shock. We know that the cycle of events is a vicious one
and at present there is no definite proof that it has its beginning in every
ease at the same spot in the cycle. Practically all authorities are con-
vineed of the fact that in severe shock there is always present a reduced
blood volume, reduced venous return to the heart with consequent di-
minished cardiac out put, peripheral arteriolar and venular vasoconstric-
tion, capillary atony as a result of either trauma or toxic substances with
consequent decreased capillary blood flow, hemoconcentration, and tissue
anozia. These changes become irreversible probably because of cither
irreparable damage to capillaries, great changes in the physico-chemical
composition of the fluids bathing the cells or failure of the compensating
mechanism to maintain sufficient blood pressure to sustain circulation in
the face of peripheral collapse.

There have been many theories concerning shock, among them the
theory that shock is due to exhaustion of nerve centers; that a toxin is
set free from injured tissues and absorbed by the blood where it causes

to the capillaries; that there is an excessive amount of CO, in
the blood stream; that there is a local loss of fluid in the injured areas in
traumatic shock sufficient to account for the fall in circulatory volume;
that severe sympathetic stimulation cither by physical or chemical means .
is sufficient to bring on the changes described above. For a full diseus-
sion of these matters I refer you to more complete monographs [Scud-
der (7), Moon (8), Harkins (9), and Cannon (10)). I do not presume
to give the complete answer to this question, but I do believe that we can
understand the problem better in the light of the changes which take
place in the peripheral vascular segment and treat it more effectively ©
with the aid of four simple tests.

I am indebted for much of what is to follow to John Seudder, with
whom I have had the privilege to be associated while carrying on clini-
eal and experimental observations related to shock.

These four tests are: (1) determination of the percentage of cells in
venous blood by means of a hematocrit; (2) determination of the spe-
cific gravity of the whole blood; (3) determination of the specific gravity
of the plasma, and (4) calculation of the content of plasmic protein by
means of a simple formula.

The merit of these combined tests lies in the speed with which they
can be done, the accuracy with which results can be reproduced, the
small amount of equipment necessary, and the ease with which the
technic may be mastered. The danger lies in attempting to interpret
these findings without a clear clinical picture of the patient.
180 Cuamzs R. Dzew.

Tae Hewatocnit

In 1885, Professor Blix presented at Upsala the first ‘‘haematokrit.”’
It was modeled after the “‘Iaktokrit’’ used in the dairy industry. Em-
ploying this method, Hedin (11), in 1891, reported an average cell vol-
ume for adult males to be 48.0 per cent, and for adult females, 48.3 per
cent. In the next ten years there were many modifications. Capps
(12), in 1908, introduced this work to America.

Haden (13), in 1923, popularized the large hematocrit tube in contra-
distinction to the capillary type and stressed the importance of using
isotonic solutions of the various anticoagulants. The publication of
Haden (14), in 1930, is very complete and for further details this article
is recommended.

In 1929, Sanford and Magath (15) modified the Haden hematocrit.
It is this tube which we prefer becanse it ean be spun in any routine
laboratory centrifuge, can be cleaned easily, and, being made of heavy
glass, its durability is enhanced.

Anticoagulant.—Heparin is the anticoagulant recommended for
hematocrit determinations. It is an active fraction of the naturally
oceurring anticoagulant which was. first isolated in Howell's laboratory

NORMAL VALUES

 

HEMATOCRIT SPECIFIC GRAVITY PLASMA PROTEIN
whole thood
pesre| | *
d*2.0270
& 48 .
Averages
EGS moos ar aterto

Cnazr 1, Reproduced from Surg., Gynec. & Obst., ‘‘Controlied Fivid Therapy** by Drew,
Beudder, and Papps, May, 1940.

by McLean (16) in 1916. The heparin now employed is the sodium salt
as prepared in the Connaught Laboratories in Toronto University,”
Canada. One milligram of the powder is sufficient anticoagulant for
the blood in a Sanford-Magath hematocrit tube. (See chart 1.)
Normal Values-—The normal values for cell volume for the male
range between 42 and 50 per cent, the average being approximately 46;
Eanty Recooxrmox axp Tazatwert or SHock 181

those for a female have a range of 39 to 43 per cent, with an average of
41,
Spzorric Gravrry or Buoop asp Praswa

The earliest investigator of blood specific gravity was Robert Boyle
(17) who, in 1684, showed that both serum and whole blood were heavier
than water. Jurin (18), in 1719, measured their weights more accu-
rately and reported the specific gravity of the blood as 1.053 and that of
the serum as 1.030. Sir John Davy (19), in 1839, determined by pyko-
nometry the specific gravity of the whole blood and quoted freely from
the earlier work of John Hunter (20), who showed that specific gravity
was high in the morning, high in inflammation, and high in dehydration.

Roy (21), in 1884, reported a simplified method of weighing blood.
E. Lloyd Jones (22, 23), in 1887, and larer in 1891, used this method and
published observations which are still of outstanding value for deter-
minations of specific gravity in both health and disease.

- Sherrington and Copeman (24) observed that a fall in blood pressure
during a long experiment or operation was accompanied by a fall in spe-
cific gravity of venous blood; hemorrhage was followed by a rapid fall,
while vasoconstriction as seen in shock caused an early rise in the spe-
cifie gravity of peripheral blood. Rogers (25) showed the value of these
tests in treating the severe dehydration of cholera.

In 1924, Barbour and Hamilton (26, 27) presented a means for de-
termining the specific gravity of body fluids which eliminated many dis-
advantages of the older methcds. The principle based on Stokes’ law
takes advantage of the fact that the time required for a drop of known
volume to fall a fixed distance through an immiscible fluid is governed by
the density of the drop and other factors, such as temperature, which
can be controlled easily. It has been shown that differences of 0.2 of 1
per cent in weight are demonstrable, and that specific gravities may be
reproduced with an accuracy of 0.0001.

Guthrie (28), in 1932, reported that, when compared with other meth-
ods for evaluation of blood conditions, it stood first from every stand-
point.

Normal Values for Specific Gravity.—In the male the average value
of peripheral blood is 1.0566 and in the female 1.0533. A swing of 0.0033
oceurs daily; the blood is more concentrated in the morning. (See
chart 1.)

Purorerss

In 1927, Atchley and Benedict (29), after a careful study of the elec-
trolytic distribution in a case of severe intestinal obstruction, suggested
that a simple determination of the serum protein might be the best aid
in following the degree of dehydration and treatment.

In 1929, Moore and Van Slyke (30) showed that there is a constant
relationship between the specific gravity of the serum or plasma and’
the content of protein. For plasma they expressed this relationship by
182 ‘ Cuamuzs R. Drew

the formula: P = 348 (G-1.0070), in which P equals the grams of pro-—
tein per 100 cubic centimeters of plasma and G equals the specific gravity
of the plasma. This work was done on human plasma and the maximum
deviation was found to be 0.6 gram per cent.

‘Weech, Reeves, and Goettsch (31), in 1936, checked the work of
Moore and Van Slyke. In their studies specific gravities were deter-
mined by pykonometry and nitrogen determinations by the micro-
Kjeldahl method. Their formula for plasma was given as P= 3401
(G-1,00687) + 0.103. It is this formula which we have used routinely.

The essence of the relationship is that plasma, completely free of
protein, has a specific gravity of about 1.00687. Only rather large

in the salt content of the blood upset this constant. The factor
of 840.1 indicates that for each increase of 1 gram per cent of protein the
specific gravity rises 1/340 or 0.00294; in other words, cach increase in
the specific gravity of 0.0001 indicates 0.03 gram per cent increase in
protein.

By this method the total protein content values are open to ques-
tion in several types of cases that have come to light so far. They are:
gross hemolysis, severe diabetes, hypercholesterolemia, gross lipemia,
and excessive bilirubinemia, but for routine, repeated studies of pro-
teins we know of no method quite sc simple, and in emergencies none
quite so rapid.

Iwrenpnetation or Vatues ix Ciovican Cases

A fairly definite idea of the history and clinical picture of the patient
should always be sought before a final evaluation is made from the data
given by the preceding tests. Most important is the trend toward or
away from normal as judged by repeated tests, and not the results of a
single set of determinations. Certain :well defined patterns have re-
curred many times in following a large series of cases, and these have
proved of great aid in the interpretation of the values in any specific
case. (Sce chart 2.)

Cutxicau Cases

Let us consider the findings in a few typical cases of shock, attempt
to interpret them, and observe the treatment dictated by the findings.

Suocx-rrose Surere Denyprariox

Cases of intestinal obstruction invariably enter the hospital with a
history of vomiting and some evidence of dehydration. Some may show
clinical signs of shock. ,

Case 1.--Ag an example T. K., a female aged 46, P. H. No. 235467,

was admitted on February 9, 1939, at 9 p.m. with symptoms and signs of
intestinal obstruction as the result of postoperative adhesions. Table 1
gives the results of the suggested tests.
Eanty Recooxrrioxw axnp Txzataest or Sxock 183

 

 

TABLE 1
Date Hour Hemewes* | Sp.Gr. Mame | iti Remarks
2- 9-39 9:00 p.m. a1 1.0307 8.10 On admission. .
2-10-39 $00 a.m. 42.0 1.0255 632 After'1500 ce. 5 per
gout gincose in se-
9-11-39 4:45 pm. 36.6 1.0238 5.78 Tmmediately follow-
: tog 1600 ce. of an-
2-14-39 8:13 a.m. 124 1.0276 7.06 Miller-Abbot Tube
working for 3
days.
2-17-39. 8200 a.m. HS 1.0271 6.86 bashes and ex-

 

 

 

 

 

 

When these findings on admission are compared with the average
normal values for women, the hematocrit suggests hemoconcentration of
approximately 20 per cent greater than normal. The protein figures are
approximately 15 per cent higher than the accepted normal figure, 7.0
Gm. per cent. In this case one may feel justified in assuming that this
patient, who had been ill for some time did not have a normal plasma
protein when her vomiting attacks began so that the 15 per cent is un-
. doubtedly on the low side. This degree of dehydration can not be
classed as severe but it is the type of warning which when heeded pre-
vents collapse later. The second tests on 2~10-39 we interpret to mean:
(1) that there was no danger of shock since hemoconcentraticn had been
reduced easily; (2) that peripheral vaseular tone was good since a
simple saline glucose solution had snfficed to relieve dehydration; (3)
that since the hematocrit value had reached normal levels while the pro-
tein level had fallen to 6.32 Gm. per cent, the patient must be suffering
from a relative degree of hypoproteinemia, which should have been
suspected from the clinical history.

The figures on 2-11-39 are of no value since the blood sample was
taken at the end of an infusion of 3,000 cc. of saline.

- The figures on 2-14-39 show values kept at close to normal in spite
of continuous suction by Wangensteen method. :

Preoperative values were considered almost ideal. No attempt has
been made here to outline the other laboratory procedures or complete
details of work up. At operation fibrous bands causing partial obstruc-
tion were incised. .

Let us consider the findings in another case of mechanical intestinal
obstruetion of a more severe type. :

Case 2.—L. P., male, P. H. No. 419165. (See table 2.)

Two findings are of great significance here. First, in spite of the
fact that the hematocrit showed only 58 per cent cells, equivalent to a
5,600,000 red blood count, the proteins indicate an increase in concentra-
tion of the fluid portion of the blood of 50 per cent. This is fast ap-
184 Cuantzs R. Dezw

IDEALIZED HEMATOCRIT-PROTEIN PAT TERNS

 

6s ao
60 as
ss ao
so 7s
4s 72
ao 6s
35 os
30 ss
25 30
20 as
SEL OUNE Pee

Cuaar 2. From ‘‘Controlled Fluid Therapy,’’ Drew, Seudder, and Pappe, Sarg., Gynec, &
Obst. 70: 859-867 (May) 1940.

Column 1. In simple dehydration, whether from lack of fluld intake, diarrhea, exesssive
Eanrzy Recocurrioy asp Turatwext or Suock 185

 

 

 

 

TABLE 2
Date Hour Hemetecelt | fp. Ce. Puma | fretcien Romerks

2-17-37 5:10 p.m. 3 1.0370 10.55 Continsous suction and

infusion.
9:40 p.m. 33 1.0379 10.55 :
10:40 p.m. 50 1.0341 9.26 ‘Still dangerous level for

operation.

2-18-37 820 a.m. 47 1.0238 5.76 =| Transfusion, then oper-

2-19-37 TOO a.m. 6 1.0283 7.28 |Good water balance;
good result,

 

 

 

 

proaching the limit which dehydration may reach without serious re-
sults. This is a real danger sign, one that neither hemoglobin, red
count, nor hematocrit alone could give. .

The second point is that after four hours, during which time the pa-
tient received a continuous infusion of saline at the rate of about 1,000
ce. per hour, the blood studies showed exactly the same values as at the
beginning. This can mean but one thing: that the fluid must have run
out of the capillary bed as fast as it went in. The vessels must have
been in the stage described as the prestatic phase with arteriolar con-
striction and capillary atony in spite of the fact that blood pressure in
this case never reached shock levels. Little has been written concerning
the ability of a very sick patient to utilize fluids. It is of great impor-
tance, and some sort of test must be used to gain this information.

Studies one hour later showed that by this time some of the fluid had
begun to remain in circulation. In addition to fluids, continuous gastric
suction was carried out. This change in the right direction eontinued.
Later when the large amounts of fluid which had leaked into the tissues.
began to return to the circulation, the proteins were too diluted, as indi-
cated by the 5.7 Gm. per cent value, and blood transfusions were re-
sorted to before exploration.

Today we would treat this type of case by administering, in order,
1,000 ce. of normal saline, then 300 ce. of 5 per cent saline in which 20-50
ce. of suprarenal cortical extract had been added and follow it immedi-
ately with 500 to 1,000 ce. of plasma. The rationale for this procedure
will be discussed a little later under Treatment.

 

Column 4. In acute changes of water balance in chronic discase, where there alrendy x-
bly a . t ot ‘:

 

iste an ia and prob , the

normal, yet the patient may go into shock from dehydration. The fluid lees in a debilitated
person, which is capable of constituents of the bloed to normal levels, may be
sufGeient to eause profound
186 Cnantzs R. Drew

It has been suggested that there are in truth only two types of shock,
one in which the changes are reversible and the other in which the
changes are not.

Case 3.—As an illustration of the second type, let me show you the
findings in the case of B. D., a woman nine months pregnant, aged 24,
who was admitted to the hospital on 10-1-38 with symptoms and signs
interpreted as evidence of a severe toxemia of pregnancy requiring im-
mediate emptying of the uterus. Contrary to expectations the improve-
ment was not marked following delivery. The patient continued to com-
plain of severe abdominal pain associated with nausea and vomiting,
’ moderately high fever, scanty urine, but with blood pressures repeatedly
within normal range. Blood studies on this patient at 4 a.m. on the
day following delivery showed : hematocrit—71.3 per cent cells; sp. gr.
plasma—1.0339; plasma proteins—9.19 Gm. per cent. These figures
were so startlingly high for a recently pregnant woman that a check was
made immediately by determining the specific gravity of the peripheral
whole blood taken from the tip of the finger and the venous blood ‘taken
from the vein in the antieubital fossa. The results were as follows: spe-
cifie gravity of finger-tip blood—1.0677 ; specific gravity of venous blood
—1.0657. This finding alone is indicative of a severe degree of periph-
eral stasis, for as Cannon (10) pointed ont following his studies in the
last World War, in severe shock the red cell count of blood taken from
the finger-tip might show several million more cells per cubic millimeter
than a sample of blood taken from the same patient at the same time but
from one of the larger veins, Soa difference in specific gravity of whole
blood from the periphery and that taken from larger veins is an i}] omen
of very serious portent. :

This patient’s blood pressure at this time was 100/80 and there were
no clinieal signs of shock, yet each of these blood findings is pathogno-
monic of a severe degree of disproportion between the peripheral vasen-
lar bed and the circulatory volume.

The clinicians in charge of this ense were advised that in the com-
bined experience of Dr. Seudder and myself we had never seen a patient
with a hematocrit showing over 67 per cent cells who had failed to go
into shock or one who had ever recovered, regardless of the treatment
instituted or the cause of the shock. ,

One liter of saline was started as soon as blood had been drawn for
testing, at 4a.m. In spite of it the blood pressure at 5 a.m. was 0/0.
At this time the hypertonic saline and “‘eschatin’’ had been obtained and
was started. By 6 a.m. the blood pressure had returned to approxi-
mately.100/80 and the bloud studies showed the following: hematocrit—
62.5 per cent cells; sp. gr. whole blood—1.0627; sp. gr. plasma—1.0275;
plasma protein—7.01 Gm. per cent. These findings suggested that ex-
ploration might be attempted since it was unlikely that the patient would
further improve. Five feet of completely gangrenous gut were found.
Another series of blood studies was done in the operating room. They
Eanty Recocysrtox axp Taratuext or Sxock 187

were as follows: hematocrit—66.2 per cent cells; sp. gr. whole blood—
1.0677 ; sp. gr. plasma—1.0267; plasma protein—6.73 Gm. per eont.

The important finding, however, was that the specific gravity of the
venous whole blood had returned to 1.0677, a figure equal to the specific
gravity of the peripheral whole blood at 4am. This indicated here, as
it has indicated in all of our experiences, a rapidly decompensating pe-

‘ripheral vascular tree. A rapid double-barreled ileostomy was done.
The patient died soon afterwards. This case never gave the clinical pie-
ture of impending collapse that these studies showed an hour before
blood pressure fell to zero. Had they been done two or perhaps four
hours earlier the changes may well have been picked up in time.

- Case 4.—The most striking response to therapy suggested in this
discussion was that of B. L., female, aged 35, who went into profound
shock on the operating table during a craniotomy for the removal of
adhesions which were thought to be the cause of epileptiform seizures.
In spite of the use of 4000 ce. of 5 or 10 per cent giucose in saline and
1800 cc. of whole blood over a period of twenty hours postoperatively,
the blood pressure had not reached a level of 60 mmm. systolic pressure.
Twenty-three hours after operation her first blood study showed the fol-
lowing: hematocrit—34.1 per cent cells; sp.. gr. plasma—1.0248; plasma
protein—6.09. .

No pulse was perceptible. No blood pressure bad been obtainable
for a period of over one-half hour. Because of the tremendous amounts
of fluids which had been given the blood studies were of little value ex-
cept to show that the profound shock was not due to hemorrhage alone
nor was it due to an insufficient amount of plasma protein to maintain
cireulation. With a large syringe, 300 ce. of 5 per cent sodium chloride
plus 20 ce. of “‘eschatin’’ immediately followed by 300 ce. of blood were
given, and within fifteen minutes blood pressure had risen to 98/60 and
was sustained at this level or better until the time of her discharge about
one month later without further therapy except for a 500 ec. transfusion
on each of four consecutive days postoperatively. This is the most un-
usual response we have seen, but in all of the cases treated to date, with
the exception of 2 with severe advanced generalized peritonitis, there
has been an increase in the blood pressure and improvement in the clini-
‘cal picture.

In some of these cases, as in the one described above, the picture of
shock again returned and the patients died. In these, undoubtedly,
changes had reached an irreversible stage.

Treatsext or Spook rnom Denypratiox

We feel that there are three basic functional derangements in the
region of the peripheral vascular segments. These are as follows:
(1) arteriolar and venular constriction; (2) capillary. paralysis; (3) loss
of fluid into the interstitial tissue.

Four things, therefore, have to be done, namely: (1) release arterio-
188 Cranes R. Drew

lar constriction ; (2) restore capillary tone; (3) return lost fluid to vascu-
lar bed; (4) maintain restored circulatory volume.

The question is naturally raised, ‘‘how can these four corrective
measures be carried ont best?’?. Experimental evidence is not available
to show specifically that any substance can directly relieve the arteriolar
spasm. It is known, however, that the severe shock seen following
burns, intestinal obstruction, trauma, marked dehydration, and cortical
insufficiency is always characterized by a loss in the plasma content of
sodium in spite of the hemoconcentration (7). Clinically it is an ac-
cepted fact that in mild cases of shock the exhibition of physiologic
saline will successfully restore circulatory volume. It scems logical to
suggest, therefore, that the first step in the correction of the above
named defects should be the introduction of finid in the form of normal
saline. If, however, the capillary bed is atonic and cannot maintain
this fluid it seems inadvisable to continue to give large quantities in an
isotonic form. It is for this reason that we suggest the introduction of
small quantities of hypertonic solutions of sodium chloride. Theoreti-
cally it should Have three effects: (1) the direct action of the sodium in
restoring electrolyte balance; (2) the direct effect of the chloride ion in
restoring acid-base equilibrium; (3) the direct effect of its hypertonicity
- in bringing back into cirenlation fluids which have already escaped into
the interstitial tissues.

There is one obvious danger in introducing any hypertonic finid into
a severely dehydrated patient. This is the danger of drawing into cir-
culation finid from the cells which is rich in both potassium and mag- .
nesium ions, each of which is extremely toxic when brought into the cir-
culation in quantities greater than those normally present in the plasma.

In correcting the second defect, that of capillary atony, experimental
and clinical evidence regarding a substance which can restore tone is
even more meager. Best and Solandt (43) have suggested pitressin.
We feel that the work of Swingle and his associates (32), Rogoff and
Stewart (33), Zwemer and Scudder (34) is adequate at least to postulate
that an extract of the suprarenal cortex not only plays a part in the re-
distribution of electrolytes but that it may have a direct action on the
capillaries and plays some role in the maintenance of their normal tone.
The clinical reports following the use of suprarenal cortical extracts
have not been uniformly encouraging. We feel that the results have not
- been as good as they might have been because the substance has not been
used in sufficient quantity. We have never seen any clinical results
when 2-5 ce. of suprarenal cortical extracts have been used, but have
had excellent clinical results with an initial dose of 10 or 20 ce. repeated
at fifteen minute or one-half hour intervals until a substantial rise in
blood pressure was obtained. We have seen no deleterious results in
these cases which could be directly attributed to the use of “‘eschatin”
(Parke-Davis) in quantities up to 150 cc. within the period of a few
hours in severely shocked individuals.
Eanty Recocmriox axp Treatwext or Sxocx 189

The third defect mentioned, the loss of circulatory volume, is geneti-
_ eally related to, and a result of, the firat two. Its correction depends
on an adequate supply of fid in a vascular bed which can keep it in
circulation. Tven hypertonic fluids will not remaiz in circulation when
the capillary bed is paralyzed.

The fourth step in the treatment consists of introducing into the
blood stream some substance with sufficient osmotic power to prevent
further leaking. The ideal substance for this purpose is blood. Plasma
is equally efficacious. Many other substances have been advocated for
the treatment of shock. Rather than diseuss them I would rather con-
tinue along this single track at present.

Suock mv Hestonnwace

The shock of hemorrhage is a more readily understandable process
than the shock in which the circulatory fluid seems to become ‘‘lost’’ in
unseen places. These four tests provide a rapid method of distinguish-
ing this type of shock from those we have just described.

Ci —In a typical case, patient G. M., female, aged 28, was ad-
mitted with the diagnosis of an acute abdomen. The diagnosis offered
some difficulty but the blood studies threw immediate light on the prob-
lem and added the final evidence to sustain a diagnosis of ruptured
ectopic pregnancy. -The blood studies in table 3 showed the following
changes during her stay in the hospital:

 

 

TABLE 3
me (he Calis) Se. Or. Ph. Gee Remarks
7-17-39 125 1.0268 6.76 Before transfusion
18.7 1.0260 6.50 omen blood and

18 212 1.0249 6.12 After 2nd transfusion.
19 2.1 1.0236 6.82 After 3rd transfusion.
2 - 333 1.0255 6.32 After 4th transfusion.

30 43.5 1.0268 6.76 On discharge.

 

 

 

 

 

I present this table to point out a rather strikingly constant finding,
ie. the relatively high level at which the plasma proteins appear to be
maintained in acute hemorrhage. ‘We have now in our records 9 cases
in which bleeding was followed by studies such as these, and in each
ease, while there was a gradual fall in the hematocrit value, there has
been relatively little fall in the protein. The explanation for this is not
clear, but we have learned to consider a falling hematocrit with a rela-
tively constant level of protein as indicative of acute hemorrhage.

TREATMENT

The treatment of such cases, when uncomplicated-by severe trauma,
is obvious. Blood transfusions should be started at once, the source of
the bleeding should be sought, hemorrhage should be stopped, and trans-
190 Cuantzs R. Dazw

fusions continued until the red cell count approaches normal levels. In
this particular case the patient reccived 500 ce. of blood before opera-
tion, 200 ce. during operation, and 500 cc. on each of three consecutive
postoperative days.

- ‘When trauma is complicated by hemorrbage the hematocrit protein-
patterns are less diagnostic, but the principles outlined for treatment
are sound, and the results are good. The base line values often cannot
be accurately interpreted, but the course of the patient can be more ac-
curately followed than by any other method we have seen.

Sock rx Burxs

, One of the most frequent canses of severe shock is that of shock as-
sociated with burns. The following table includes studies made on case
6, C. P., male, aged 45, P. H. No. 519132. This case has been reported in
some detail by Seudder in his book on ‘‘Shock.’? I present it to point
out two things. Onc, hemoconcentration, which is well known and well
recognized; the other, hypoproteinemia, which is still too little thought
of when the treatment of burns is considered. Table 4 gives the studies
for the first three d.ys on the blood of a severely burned man and will
serve to point out these two points: .

 

 

TABLE 4
Dote Heer "eau Se. Gr. FL oh

5-72-37 955 p.m. 66.7 1.0235 5.96
11:50 p.m. 62.7 1.0245 5.99
8  -7:38 as. 508 1.0215 498
1225 p.m. 53.8 1.0215, 4.96

9 6:30 a.m. $2.2 1.0222 52

1:00 pan. 513 1.0223 53

 

 

 

 

 

Underhill and his associates (35) probably should receive the credit
for bringing forcibly to the attention of surgeons the important role of
fluid loss in burns. Davidson (36) in 1927, revolutionized the treatment
of burns when he introduced the tannic acid method. Aldrich (37), in
1933, showed that most of the so-called toxemia of burns is probably at-
tributable to infection. Only recently have the roles which proteins
play been given adequate recognition. Harkins (38), following David-
son at the Henry Ford Hospital, has done much to bring this phase to
the attention of the profession. Table 4 gives a fair idea of the levels
to which the proteins may fall even before the administration of fluids.
It also shows that with fluid therapy the protein level is likely to go
below not only the latent edema level of approximately 5.5 grams per
cent but also below the true edema level of approximately 5 grams per
cent. One cannot conceive of a happier hunting ground for anerobic
Kanty Recocwrrios anv Treatsmyt or SHock 191

bacteria than the soggy, edematous, badly injured tissue beneath a pro-
tein coaguiam created by tannic acid, silver nitrate or some other co-
agulating substances. In the treatment of burns, therefore, especially
in the treatment of shock, which is so dominantly a feature soon after the
accident, it is not only necessary to prevent pain, prevent heat loss, in-
sure adequate oxygen, and prevent further loss of fiuids and proteins,
but it is imperative that the proteins already lost be restored. The
ideal substance for this purpose is plasma or serum either in liquid form
or by means of solutions of dried forms. It not only will decrease
hemoconcentration by restoring fluid but at the same time will sustain
the protein level and cirenlatory volume. Several formulas (39, 40,
41) have been worked out in an effort to define the amounts of plasma
needed in any specific case. The only difficulty with formulas is that
they work so well on normal adults with perfectly intact peripheral
vascular systems and work so poorly on very ill individuals in whom the
circulatory volume, the vascular bed capacity, and the concentration of
the blood elements become almost a function of the state of the terminal
vasenlar segments; that is, they become a function of a very decidedly
unknown quantity. For instance, in a series of experiments carried out
on unwilling colleagues and patients who were not too ill, it appeared
that fluid balance in a dehydrated patient might be accurately re-estab-
lished by giving 50 ec. of normal saline intravenously for every 0.01
gram of plasma protein above the arbitrarily normal value of 7 grams
per cent. As an example, a patient who has been vomiting until the
plasma proteins register 7.5 grams per cent can be restored to normal
very easily by giving him 2,500 ec. of normal saline. The only difficulty
is that a patient in profound shock may be given 2,500 ce. of normal
saline and blood studies at the end of the infusion may show values
higher than at the beginning. This point, too, has not been stressed
cnongh. It is as useless to continue to pour fluids into a vascular sys-
tem which cannot hold them as it is to feed carbohydrates to a severe
diabetic unless each of these procedures is controlled by some method of
checking the ability of the individual to handle these substances. So it
is with plasma. We have found that the average individual of about 60
kilograms of body weight will require approximately 1 liter of plasma
to raise the plasma protein levels 1 gram per cent. This is a very
rough figure but a very useful one. In severe shock, in severe infec-
tions, and in marked hypoproteinemia, the quantities given must be con-
siderably increased and one must never assume that the injected mate-
rial has remained in circulation unless the values are actually checked.
Treatment, therefore, is similar to that described under dehydration,
except that fluids should be given much more carefully and whole blood
is less ideal than plasma.

Suaoox rx Pezrroxrris

There is a great similarity between the shock of a severe burn and
the shoek in severe peritonitis. The area of skin is just about equal to
192 Cuantes R. Drew

the area of the peritoneum in any given individual. Just as the area of
the skin involved in a burn is a real factor in the eventual outeome, so
the area of the peritoneum involved is a real factor. ‘When the skin is
irritated by a physical agent such as heat there is capillary ectasy and
loss of protein-rich fluid to the exterior. When the peritoneum is irri-
tated by bacterial toxins there is also a great loss of protein-rich fluid,
az well as the loss of power of absorption. The end result in each case
is the same. There is marked hemoconcentration, dehydration and
hypoproteinemia. Each of these we know may play some part in the
production of shock. As a typical illustration, case No. 7, E. D., fe-
male, age 64, P. H. No. 561768, is presented.

This patient was admitted with a diagnosis of carcinoma of the
stomach which means that she, like all of the other patients suffering
from a similar malady, was anemic and relatively hypoproteinemic on
admission. We have no preoperative blood studies, but following
gastrectomy there was some leakage in the region of the dnedenum,
peritonitis and subsequent duodenal fistula. Table 5 presents graphi-
cally the changes in her blood picture brought about by the use of blood
transfusion, plasma, protein hydrolysates, and intensive vitamin and
sulfanilamide therapy, in an attempt to control the irritant, restore fluid
balance, remove the edema, and return the gastrointestinal tract to nor-
mal activity.

 

 

 

TABLE &

Date Hematocrit Sp. Gr. Pl. Protcins | Remarks
Ines 50.4 1.0203 456 Marked edema
121789 53.9 1.0210 4.79
1/28/88 518 1.0207 4.69
1/25/88 44.0 1.0217 436
127789 40 1.0226 534 Edema gone

 

 

 

 

Here one notices the same hemoconcentration, though not as marked
as in the case of the burn because the initial red cell count undoubtedly
was much lower than that of the healthy male who was burned. On the
other hand, the change in percentage is probably greater. The protein
level is definitely below the edema level and this becomes a doubly im-
portant factor in the surgery of the gastrointestinal tract. Soggy
wounds will not heal; sutures, if of silk, pull out of the water-logged
tissues, and if of catgut, the tensile strength is diminished to the point
where rupture is more likely. Peristalsis is slow or disappears entirely
. leaving a paralytic ileus with its attendant train of complications as the
result of the mechanical effects of distention. Only careful and re-
peated checks as a guide to therapy can salvage some of these difficult
cases,
Eanty Recooxrros axp Treatuest or Siock 193

Broop Srupies rs Heap Issunmes, Curst Suncery axp AsesrHesta

Attempts so far to correlate the results of hematocrit-protein pat-
terns in cases of severe head injuries and in major chest surgery have
not been very successful. The effect of raised intracranial pressure on
the peripheral vascular tree in our experience has been a very variable
one. Attempts to correlate changes in the specific gravity of the cere-
brospinal fiuid with the degree of damage done to the brain have not
yielded usable results. Changes in intrathoracic preasure with its ef-
fect upon the large vessels likewise cause systemic upsets which we have
not yet been able to measure in terms of hemoconcentration of the blood.

Attempts to establish a relationship between peripheral cireulatory
changes and the various types of anesthesia have not advanced to the
point where they may be stated with authority. In this field we feel
that these simple tests offer tools which may be used to great advantage
in anesthesia.

~ No attempt has been made in this discussion to cover shock in all of
its many ramifications. But we do believe that with a constant clinical
picture of the patient in mind, a working concept of the changes which
take place in the physiology of the body under the stress of various de-
grees of irritation, particularly the changes which take place in the pe-
ripheral vascular tree, cases of shock will be more adequately handled.
With the aid of such a series of simple tests as we have attempted to ont-
line here, impending troubles may at times be foreseen and prevented
altogether.

Susrarany

(1) Changes in the peripheral vascular tree of a segmental nature as
observed by Ricker and Oertel are presented as a basis of better under-
standing the mechanism of circulatory failure in surgical shock.

(2) On this basis, there are three defects in the peripheral vascular
tree which need correction in shock. These are: (a) arteriolar and
venular constriction; (b) capillary dilatation; (c) stasis of cireulatory
fluids in the capillary bed or loss into the tissue.

(3) To correct these defects three steps are recommended: (a) aid
in the restoration of the electrolyte balance, acid base equilibriam, nor-
mal arteriolar tone and circulatory volume by use of intravenous sodium
chloride, at first in isotonic form and then in hypertonic form if there is
no response to the former; (b) aid in the restoration of capillary tone
by using water soluble suprarenal cortical extract in quantities sufficient
to get a response in blood pressure; (c) sustenance of circulation by ade-
quate amounts of blood or plasma.

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