THE SEQUELÆ OF ANÆSTHESIA.
Respiratory System.
After operations performed under any form of anæsthesia, even spinal,
there is always a possibility of pneumonia or bronchitis. The
anæsthetic itself is not always to blame. The patient has suffered
trauma and is confined to bed, and may develop a hypostatic pneumonia
just as a person who has suffered from a fractured thigh so commonly
does, even though he has had no anæsthetic at all.
It is probable that organisms, capable under certain circumstances of
causing inflammatory disease of the respiratory tract, are present
in a large proportion of apparently healthy people. Pneumococci and
streptococci of varying strains may be grown from nasal or pharyngeal
secretions of patients who suffer from catarrh of these regions, and
may reappear upon slight provocation even when prolonged treatment had
apparently banished them permanently. All that is required to start
an acute infection of lungs or bronchi, is some factor that depresses
vitality and lowers body resistance to the organism. And if in addition
use has been made of an inhalational anæsthetic such as ether, which
may cause an immediate and fairly acute congestion of the respiratory
mucous membranes, it is not to be wondered at that serious sequelæ
follow in a certain proportion of cases.
Laboratory results go to show that ether lowers the opsonic index
of the blood to pneumococci and streptococci, but without placing
undue emphasis upon a mere isolated phenomenon such as that, it is
plain that the whole conditions of the patient after operation are
favourable to the occurrence of pneumonia or bronchitis, and that of
all anæsthetics ether is the most likely to be the determining factor.
Experience gained during the war has thrown a certain amount of light
upon this subject. Post-anæsthetic bronchitis and pneumonia was
very prevalent among the wounded, far more so than among civilian
patients. It is, the author believes, reasonable to attribute this
fact to several causes. In the first place, the soldier’s life,
alternating between stuffy billets and wet trenches, predisposed him
to naso-pharyngeal catarrh of a fairly high degree of infectivity.
Enthusiastic press representatives might state that you could not take
cold so long as your feet and legs were always buried in half frozen
mud, but experience hardly bore out their golden promises. Again, the
soldier did not improve his catarrh by inveterate cigarette smoking.
Lastly, military hospitals were large institutions, some under canvas,
some in huts, some in buildings constructed for other purposes, and
rapidly altered to the urgent needs of the army. Of whatever type,
nearly all had one feature in common--many of the surgical wards were a
long (and draughty) way from the operating theatre.
For the prevention of post-anæsthetic pneumonia, the author offers the
following tentative suggestions:--
(1) See that the skin is kept covered up as much as possible
during the operation and that the patient is not exposed to
draughts during or after it. Rooms can, and should be, well
ventilated without cold draughts.
(2) If a patient has an acute or sub-acute naso-pharyngeal
catarrh, treat it as fully as possible before operation by
sprays and gargles.
(3) Do not use ether to patients who suffer or recently have
suffered from such conditions.
(4) Give a hypodermic of morphia and atropine before operation
as a routine.
(5) In so far as possible, let the patient’s shoulders and head
be raised by pillows during the early hours of convalescence.
(6) Lastly, remember that while no care will absolutely banish
these dangerous sequelæ from our practice, the greater care
and skill shown by the anæsthetist, the less bronchitis and
pneumonia will appear among his patients. As regards ether, the
author believes that it is the strength of vapour used, more
than the duration of the anæsthesia, which counts. It is for
that, among other reasons, that he has for the induction period,
no hesitation in recommending a method whereby a small part of
the requisite ether strength is replaced by chloroform.
Vomiting.
After an anæsthesia lasting more than a few minutes, it may almost be
regarded as normal for the patient to vomit once or twice. Usually this
occurs a few minutes after the administration has ceased. In the case
of nitrous oxide and oxygen, even this slight disturbance may not occur.
The amount of vomiting which after this stage may be regarded as
normal is difficult to determine. The author took notes of some 300
cases on this point. The details of his results are not suitable for
a text book, but, broadly speaking, it would appear that after an
operation of ordinary duration and severity, the vomiting returns on
the average some five or six times, and usually ceases on the evening
of the operation day. A limited number continue to vomit at intervals
until the early hours of the following morning. With nitrous oxide
and oxygen the vomiting is far less than the above, though even with
this anæsthetic quite severe emesis may occur. With closed-ether, the
trouble is very violent for a short time, large quantities of mucous
being ejected: it is probable that after the first two hours, it is no
more marked than after open methods. The use of morphia and atropine
before operation most certainly reduces the violence and duration of
this sequela.
Prolonged more than twenty-four hours, the condition must be regarded
as definitely abnormal.
PREVENTION AND TREATMENT.
The adoption of open-ether preceded by morphia and atropine and due
skill and thought on the part of the anæsthetist, combined with proper
preparation of the patient, are the only means of prevention at our
command.
The raised position of the head and shoulders during the recovery
stage undoubtedly tends to reduce the nuisance. It is a vexed question
whether to give or to withhold fluids after operation--and this matter
is of course in the hands of the surgeon, not the anæsthetist. In
certain cases, the author believes that it is worth while trying the
effect of a cup of fresh tea with very little sugar or milk. Even if
rejected in a few moments, the astringent effect of the infusion seems
to soothe the gastric mucous membrane, and give relief.
Post-operative Acidosis.
(Synonym--Delayed Chloroform Poisoning).
In a limited number of cases, post-operative emesis assumes a grave
type, and definitely threatens life. Such cases began to be studied
in the early part of this century, and though our knowledge of the
condition is still incomplete, the student should be acquainted with
the present views held upon the subject.
Clinically, the earliest symptom to raise suspicion, is the
reappearance of vomiting at a time when one would expect such trouble
to have abated, usually twenty-four or thirty-six hours after
operation. Within a few hours, the nature of the vomit changes from
the usual bilious stomach contents, and shows obvious evidence of
the presence of _altered blood_. The pulse and temperature begin to
rise, the countenance assumes an anxious look. A trace of jaundice is
usually present. The nervous system becomes affected as shown first in
restlessness, and later, delirium. Every degree of this condition is
possible, but a very large proportion of recognisable cases pass into
coma, and death supervenes within a few days, sometimes less.
Investigation into such cases has shown that the essential underlying
condition is an acidosis closely allied to that seen in diabetic coma.
The breath has the peculiar sweetish aroma of acetone, and acetone,
diacetic acid, and B. oxybutyric acid successively appear in the urine.
Post-mortem, the most striking change found is a profound fatty
degeneration of the liver, the cells of which are disintegrated as in
acute yellow atrophy.
It is obvious from the foregoing that there is present a very
remarkable abnormality of metabolism. Mr Rendle Short, in his admirable
book, _The New Physiology in Surgical and General Practice_, gives
the following explanation of the condition:--
“The physiological process of dealing with fat is to resolve it into
carbon di-oxide and water. If we make a pound of fat into tallow
candles and burn it, we shall obtain carbon di-oxide and water, and a
certain amount of heat will be evolved. If the pound of fat is eaten
and absorbed by a man or an animal, it will be burnt to the same end
products, and the same amount of heat will be given out. But in certain
circumstances, an abnormal mode of breaking down is followed, and
there are produced, first B. oxybutyric acid, then diacetic acid, and
finally acetone. If this takes place on a large scale, the conversion
into acetone fails to keep pace with the production of acids. Therefore
first acetone appears in the urine, then diacetic acid, and finally
oxybutyric acid; the last may rise rapidly to an enormous figure: 30,
50, or even 180 grams may be passed daily.”
Later in the same chapter, Short propounds the question as to what are
the special circumstances in which the breaking down of fat deviates
from its normal course, and follows this dangerous route. The answer
is, he says, quite definite and decisive. When the tissues are unable
to obtain sugar from the blood, fat is broken down _via_ these
dangerous acids to acetone, instead of to carbon di-oxide and water.
Such an inability on the part of the tissues to obtain sugar arises
under several conditions:--
(_a_) In diabetes, where sugar though freely present in
the blood cannot, for some reason still not clearly known, be
assimilated by the tissues.
(_b_) In poisoning by salicylates.
(_c_) In starvation, for obvious reasons. The supply of sugar
from the liver has been used up, and the patient, living on his
own fats, breaks them up abnormally.
(_d_) In post-anæsthetic poisoning, for reasons which are
at present not clearly ascertained.
Upon the theoretical side it is therefore not possible to say more than
that anæsthetics sometimes initiate this abnormal metabolic process. To
the question as to why and how they do so, we can as yet give no answer.
Upon the practical side, we can, however, speak much more definitely.
Acidosis follows the use of ether very rarely indeed: after nitrous
oxide it is unknown. Chloroform has been the drug used in almost every
recorded case, while ethyl chloride has been responsible in a few
isolated instances. Young children are much more prone to suffer than
adults, though the author had a fatal case in a lady well over forty
years of age: he has also seen a case very nearly fatal in a soldier
aged twenty. This man was, a week after recovery from acidosis,
anæsthetised for half-an-hour with nitrous oxide and oxygen, without
exhibiting any signs of a return of his dangerous condition. Anæsthesia
repeated in the same subject after a short interval is more prone
to start the process than a first inhalation. Lastly, acute sepsis,
particularly in the young, is notorious for its liability to be
followed by acidosis.
PREVENTION AND TREATMENT.
The obvious moral of the foregoing is that chloroform should not be
administered to patients suffering from acute sepsis, particularly if
they be very young. Indeed, so common is a mild degree of acidosis
among children, some surgeons consider there is a definite risk in
giving chloroform to them at all unless special precautions are taken.
Chief among these are regular dosage for a day or two before operation,
with considerable doses of bicarbonate of soda and sugar, which is a
routine measure in some children’s hospitals.
As regards curative treatment, much can be done if the gravity of the
condition is recognised early. The stomach is first washed out with
alkalis, and a substantial dose (one dram) of bicarbonate of soda left
in it. The same dose is repeated hourly by the mouth, if retained, or
per rectum. A useful addition to the alkaline treatment is dextrose,
also in teaspoonful doses. In grave cases, these drugs should be given
intravenously in saline solution.
These measures combined with warmth, and ample fluids by mouth or
rectum, will often save life, but to be of any value they must be
begun early. Fulminating cases occur which succumb rapidly in spite of
treatment.