SHOCK AND ANÆSTHESIA.
Under this short and convenient title, the author proposes to discuss
all the changes observable in the patient’s condition, the causation
of which can be traced to the procedure of the surgeon. The use of
the term _shock_ was at one time, and by some teachers still is,
restricted to a definite clinical condition. The patient was described
as lying pallid and almost pulseless, with dilated pupils, cold
sweating skin, and gasping, irregular respirations. In the view more
generally taken to-day, that is but the extreme and final manifestation
of a syndrome, which any patient who suffers trauma (whether inflicted
accidentally or by the surgeon) exhibits in a greater or less degree,
and from which general anæsthesia protects a patient to a very limited
extent only.
Professor Crile, to whose work we owe so much of our knowledge on this
subject, has said, “In general anæsthesia, part of the brain only is
asleep.” Though consciousness is abolished, many parts of the brain
are quite capable of responding to _centripetal impulses_ passed
to the brain through sensory nerves injured by the knife. A full
account of the changes demonstrated by Crile in some of the cells of
the grey matter of the brain as a result of such stimuli, and of the
interpretation put upon these by their discoverer, is not suitable for
a text-book of anæsthesia. It is sufficient to say that such changes
have been discovered, and that their occurrence as a result of trauma
is not prevented by inhalational anæsthesia. Such changes, though of
the utmost interest scientifically, cannot be demonstrated clinically,
and it is to alterations of _blood pressure_ and of _respiration_ that
we must look for clinical evidence of the effects of _shock stimuli_.
[Illustration:
FIG. 1.--Shock--Blood pressure of a dog undergoing
laminectomy under general anæsthesia (Grey and Parsons.)
(_Reproduced by kind permission of the Authors._)]
With every incision by the surgeon, sensory nerve twigs are of
necessity injured. The fibres found in sensory nerves are, it will
be remembered, either pressor, or depressor--that is, stimulation of
them, causes either an increase or decrease of the blood pressure,
the depth and frequency of respiration being usually affected in the
same direction as the B.P. That such changes do commonly occur is
easily recognised by clinical observation. The veriest beginner in
anæsthesia soon learns to expect a deeper, quicker respiration and a
stronger pulse as soon as the operation has begun. These changes have
been studied experimentally upon animals and upon the human subject by
the use of the sphygmomanometer: Fig. 1, drawn from Grey & Parson’s
Arris and Gale Lectures of 1912, shows a tracing from a dog undergoing
laminectomy under general anæsthesia, and gives a good idea of the
early evidences of shock.
* * * * *
We may condense the results of much work on this subject under the
following headings:--
(_a_) Most stimuli from the field of operation cause a
sharp rise of blood pressure, followed by a sharp fall.
(_b_) Successive stimuli delivered quickly one after
another add their effects together, the total result being
considerably greater than from one severe trauma.
(_c_) After a time, the pressor effect of stimuli begins
to lessen: the animal or patient “wears out,” and finally no
pressor result can be obtained by the most massive stimulation:
the curve of B.P. steadily falls: the condition of full surgical
shock is produced.
(_d_) The tearing or pulling of tissues produces more
powerful stimuli than the use of a sharp knife, and, therefore,
brings on the full condition of shock more rapidly.
(_e_) Stimuli from some tissues cause much more reflex
effect upon the organism than from other less sensitive
structures. This is well exemplified when an abdominal section
is in progress. Incision of skin causes immediate response in
deepened respiration and higher B.P.: division of the fascia
very little effect. If the muscle is divided by the knife, again
little reflex effect is noticeable, but if it be stretched and
split by the fingers, the response is powerful. The parietal
peritoneum, however delicately handled, is one of the most
sensitive structures in the body, and, unless the patient is
fully under at the stage either of opening or closing this
layer, actual breath-holding or straining will occur. On the
other hand, incision or suture of the hollow viscera will cause
practically no response however light the anæsthesia, provided
these structures, and their connections with the parietes, are
not pulled upon.
(_f_) Stimulation of certain selected areas, of which the
spermatic cord is a well-known but by no means the only example,
results in an almost immediate fall of blood pressure with
little or no preliminary rise. In the operating theatre, we
sometimes see faintness or syncope arising quite suddenly during
operations in such regions. This subject is explained more fully
in Chapter XVI. under the term “Reflex Syncope.”
Illustration:
FIG. 2.--Combined blood pressure chart showing
the average of a number of experiments.--A--Under nitrous
oxide and oxygen. B--Under ether. At each spot marked
x, a trauma (burning of the paw) was inflicted. (After
CRILE.)]
(_g_) While no general anæsthetic protects absolutely
from shock stimuli, some anæsthetics give more protection than
others. Nitrous oxide is the most effective in this respect,
its powers being two and a half times greater than that of
ether: chloroform is even less effective than ether (_see_
Fig. 2).
(_h_) The claim made by the older generation of surgeons
that shock could be prevented by the use of a _deep_
anæsthesia, and that the occurrence of any “Reflex syncope” was
always a sign of too light an anæsthesia cannot be made good. At
the same time, it must be admitted that too light an anæsthesia
does increase the likelihood of shock. _Prolonged deep_
anæsthesia, on the other hand, produces by itself a condition
indistinguishable from shock, with the single exception of
nitrous oxide gas.
(_i_) Operative shock is predisposed to by several factors
of which the following are the most important:--
1. Hæmorrhage before or during operation.
2. Sepsis.
3. Fear.
4. Prolonged starvation.
5. Certain diseases, especially hyperthyroidism
(exopthalmic goître).
Theories of Shock.
So far as we have touched in the above upon theory, it has been theory
which receives general acceptance and which accords with known clinical
facts. When we come to discuss _the reason why blood-pressure falls
in shock_, we are in more debatable country.
Crile’s original view was that the upstroke seen in such charts as
shown in Fig. 1 are caused by reflex vaso-constriction, and that the
final fall of B.P. was due to exhaustion of the vaso-motor centre.
This view he does not seem to have modified as a result of his later
discovery of degenerative changes in certain cells of the grey matter
of the brain.
Other workers, J. D. Malcolm in this country, and Yandell Henderson,
of Yale, U.S.A., maintain an opinion diametrically opposite. In their
view, in fully developed shock, the vessels are in vaso-constriction,
and the circulation is arrested from undue internal resistance to blood
flow.
A third explanation of lowered B.P. has been offered, and while its
significance is not understood, there is fairly general agreement as
to its validity. This factor is a _reduction in the total blood
volume_--an oligæmia. No one has as yet demonstrated to what region
or organ the missing blood volume has retreated.
YANDELL HENDERSON’S ACAPNIC THEORY OF SHOCK.
Acapnia is a condition in which the CO_{2} content of the blood and
tissues has been brought to too low a level. Those who climb mountains
suffer from it, and so do those who breathe rapidly and heavily for a
prolonged period. Carbon dioxide is necessary for the vigour of the
respiratory centre, of which it may be termed the natural regulator.
Moreover, the heart and the great veins which empty into it require a
certain proportion of CO_{2} in the blood.
Admittedly, patients inhaling anæsthetics do on occasion breathe too
deeply. Sometimes they do so voluntarily before losing consciousness,
sometimes reflexly as a result of such a manœuvre as stretching the
sphincter ani. Do they thereby bring their CO_{2} down to a level which
does serious harm and which can be considered a cause of collapse under
anæsthesia? Henderson says they can and do: most other workers deny the
possibility.
[Illustration:
FIG 3.--Diagram (after CRILE) to illustrate
anoci-association. In “A” the trauma is inflicted on the leg,
and the brain being wholly unprotected, considerable shock
is suffered. In “B” the brain is protected by inhalational
anæsthesia from the effects of fear, etc. In “C” the sensory
nerves from the seat of trauma are blocked by novocaine,
and the brain also protected by inhalational anæsthesia.
Theoretically no shock is suffered.]
Prevention and Treatment of Shock.
There are many theories of shock but only one anti-shock technique
which will bear examination. Founding upon his own theory, Crile about
1913 elaborated his ANOCI-ASSOCIATION method of which the
following are the leading features (_see_ Fig. 3):--
(_a_) _Prevention of fear._--Every member of this team is taught
the all-important art of so dealing with the patient that no
unnecessary fear is allowed to remain in his mind. That art does
not consist in endless repetition of the phrase, “Do not be
frightened,” but rather in each so bearing himself or herself
before the patient that he may gradually acquire the conviction
that he is surrounded by careful, kindly, and skilful persons
who are doing for him what they do for hundreds of others, and
doing it with an expectation of his early and complete recovery
so certain that they do not need to put it into words unless
definitely questioned. Such an art is not acquired in a day, and
some unhappy few are so constituted that they can never acquire
it.
As a further preventative of fear, and also for other reasons
explained in Chapter vi., the patient receives a dose of morphia
(⅙th grain, with ¹⁄₁₂₀th grain atropine, hypodermically) three
quarters of an hour before operation. Some surgeons go further,
and give a sedative the night before operation. Veronal gr.
viii. is the favourite prescription of Prof. Alexis Thomson of
Edinburgh.
(_b_) The sensory nerves are “blocked” by infiltration with
novocain. By the systematic use of local in conjunction with
general anæsthesia, the harmful stimuli from the area of
operation are prevented from reaching the brain. For the details
of this measure, the reader is referred to Chapter xx.
(_c_) The anæsthetic of choice in Crile’s practice is nitrous
oxide and oxygen (_see_ Chapter vii.).
The whole of this technique has not been generally adopted as a
routine, but nevertheless the teachings of Crile have greatly
influenced the mind and practice of most surgeons and anæsthetists.
Traces of that teaching are to be found everywhere in the organisation
built up during the Great War to save as many as possible of the lives
of badly smashed men. At no previous time in the history of surgery was
the problem of shock so pressing, and a brief resumé of the methods
adopted is here set down, as an example of how shock should be dealt
with.
[Illustration: FIG. 4.--Lane’s apparatus for
subcutaneous infusion of saline solution.]
Treatment of Shock among the Casualties of the War.
The first essentials demanded were the most careful organisation, the
provision of equipment far in advance of most home civilian hospitals,
and of surgical teams specially trained to a high level of excellence.
Upon recovery from the field, the injured man received at the ADVANCED
DRESSING STATION, such first aid dressing as was necessary, and a
substantial dose of _morphia_. When the latter had had time to take
effect, the case was passed back to the Field Ambulance (where he
received his first dose of antitetanic serum), and from there to the
CASUALTY CLEARING STATION. During every stage of the journey, he
received as much _warm fluid nourishment as possible_. Arrived at
the C.C.S., the severe case was passed first into the RESUSCITATION
WARD. This department, under the charge of a specially trained M.O.,
concentrated largely upon two measures--the thorough _warming_ of the
patient, and the replacing as far as possible of the fluids lost to
him by hæmorrhage and shock. The warming in many C.C.S.’s was effected
by electric radiant heat baths. The fluids were replaced either by
way of infusing blood from another patient, or by the use of _gum
saline solution_. Introduced into a vein, the action of this solution
persists for a much longer period than that of ordinary saline, being
less easily lost by osmosis through the capillaries into the tissues.
From the resuscitation ward, the patient passed to the OPERATING
THEATRE. Though the full technique of anoci-association was not always
possible, the maxims which Crile had sought to inculcate into the
practice of surgery influenced the work of surgeons and anæsthetists
very profoundly. Nitrous oxide and oxygen was used for all the severely
shocked cases, and infiltration with local anæsthetics where feasible
and necessary.
Subcutaneous Infusion of Saline.
For those who do not feel bound to adopt the Crile technique this is a
simple measure which does much to minimise shock in prolonged abdominal
operations. Saline infusion into a vein is so rapidly excreted that its
influence is very fugacious, but if the fluid be introduced under the
skin during the period of operation it is slowly absorbed as required
by the blood. Sir Arbuthnot Lane is a strong advocate of this measure.
Fig. 4 shows a suitable apparatus. The needles are thrust into the
loose areolar tissue under the breast, one on each side, and a pint or
more of fluid is _slowly_ run in from the reservoir.