CHAPTER XVI.

THE ACCIDENTS OF ANÆSTHESIA.

The minor difficulties of anæsthesia have already been dealt with,

and if the instructions already given, particularly in Chapter

III., are faithfully carried out, incidents of real danger

will rarely occur. The soundest knowledge and the most conscientious

care will, however, never entirely rid anæsthesia of an element of

danger to life. The conditions now to be considered are:--

(_A_) Vomiting.

(_B_) Failure of respiration.

(_C_) Failure of circulation.

(A) Vomiting.

This always exposes an unconscious patient to the danger of inhaling

solid or fluid material into the larynx, with resulting asphyxia. If

the patient be tided through that immediate difficulty, he is liable to

develop an inhalational pneumonia subsequently.

A healthy patient properly prepared should not vomit during the

induction stage, nor during the progress of the operation. If he

does, it means that the induction has been too slow, or that the

administration has been intermittent, and the patient has been

permitted to come to too light a level of anæsthesia during the

operation.

During emergency operations where the patient’s stomach may be full of

food, the case is different. Such patients commonly vomit early in the

induction stage, and no skill can avert the incident.

A patient suffering from intestinal obstruction, or from generalised

peritonitis has his stomach and intestines full of highly infective

fluid. Reverse peristaltic may set in merely as the result of the

inhalation, or later from handling the contents of the abdomen, and

the feculent fluid gushes up the œsophagus with little or no warning.

Since vomiting in these cases may occur even in deep anæsthesia, when

the cough reflex which is the normal sentry to the entrance of the

larynx, is abolished, the dangers of insufflation are very real indeed.

Personally, the author prefers to wash out the stomach before beginning

to induce anæsthesia in these cases, but some surgeons believe that the

shock of this procedure outweighs the advantages.

SYMPTOMS AND TREATMENT OF VOMITING.

In ordinary cases, vomiting is usually heralded by a definite train of

symptoms. Respiration becomes shallow, the colour a little pale and the

pulse rather small. The pupil dilates, but remains active to light,

indicating that the alteration of respiration and circulation is not

due to overdose.

At the first appearance of such symptoms, a brisk rub of the lips and

thereafter an increase of the vapour strength of the anæsthetic will

often avert the impending vomiting by deepening the anæsthesia, but if

the possibility of this complication has occurred to the anæsthetist

too late for its prevention, the head must be turned well to one side,

and the other shoulder slightly elevated by a pillow, so that vomited

material will fall out of the mouth at once. When the actual act of

vomiting is over, no time must be lost in mopping out the mouth and

pressing on with the production of a deeper anæsthesia.

(B) Respiratory Dangers.

These divide themselves into two groups:--

(1) MECHANICAL.--The respiratory movements continue, but the

ingress and egress of air is blocked.

_The symptoms and preventative treatment_ have been referred to at some

length in Chapter III., and no further account of these is therefore

necessary. _The treatment of a complete blockage_ of the air passages

which resist the measure there described, alone remain to be mentioned.

Of these, the only two effective are _artificial respiration and

tracheotomy_ (or laryngotomy if preferred by the surgeon). Forcible

artificial respiration by the Sylvester method, with the mouth gagged

open and the tongue held forward by the tongue forceps, is frequently

successful in getting over even a complete block, but the last resort

of opening the air passage by the knife must not be delayed until too

late. In deciding such a point, considerable judgment is of course

called for.

(2) NON-MECHANICAL.--Respiratory arrest.

This is usually seen in conjunction with a serious failure of the

circulation caused by over-dosage. Exceptionally, some act of the

surgeon sets up a reflex inhibition of the respiratory centre; the

circulation is at the same time depressed, but to a varying degree.

The cardinal _symptom_ is arrest of all respiratory effort. The

_treatment_ is best dealt with under the heading of circulatory

failure.

(C) Circulatory Failure, or Syncope.

By the term syncope, we mean a more or less sudden failure of the

cardiac pump, as opposed to the form of circulatory failure seen in

surgical shock, where the condition is chiefly, though not wholly, one

of vaso-motor paralysis (_see_ Chapter II.).

Syncope occurs under varying conditions which may for descriptive

purposes be divided into four classes. It is not, however, always

possible to decide with certainty into which class an individual case

should be placed.

The _symptoms_ common to all classes of syncope are:--

(1) Pallor, and loss of all tone in the muscles, noticeably

those of expression. The pulse is weak or imperceptible.

(2) Cessation of respiration.

(3) Dilatation of the pupil, which ceases to react to light.

The four classes above mentioned are as follows:--

A. PRIMARY SYNCOPE.

This is peculiar to chloroform. With no other anæsthetic is it seen, at

any rate in the healthy subject. It arises during the induction period,

and is not necessarily preceded by any respiratory difficulty. There is

one big inspiratory gasp, sudden and extreme pallor, and the pupil goes

out to the rim in a few seconds. The only reasonable explanation of

such an incident is the occurrence of vagal inhibition (_see_ page

112). Its prevention therefore is a matter of the avoidance of a high

percentage of chloroform.

B. SECONDARY SYNCOPE.

This term is applied to a collapse arising as a secondary result of

embarrassed respiration. Though not peculiar to chloroform, it is

far more common with that drug than with any other (ethyl chloride

excepted). The most common time for the accident is towards the end

of the induction period. The patient has probably been struggling,

has clenched the jaws, and developed “mechanical” asphyxia. Violent

inspiratory efforts are still being made, and considerable cyanosis

develops. Either at the very moment when the respiratory difficulty

is overcome, or while it still persists, the colour suddenly alters

from blue to white, and the other symptoms of syncope rapidly appear.

The exact period required to transform a blue struggling patient with

heaving chest, into one with pallid face, and motionless chest and

limbs, varies greatly, for reasons furnished below.

The most reasonable explanation offered of such an accident is that

given by Leonard Hill. The attempts to inspire through an air way

mechanically blocked cause an immense strain upon the heart muscle. The

flow of blood in the lung capillary is hindered, and the right side of

the heart becomes over distended with blood. Its musculature is further

damaged by the fact that the blood in the coronary vessels is deficient

in oxygen, and that a considerable dose of anæsthetic has already been

absorbed. There is the further fact, not mentioned by Hill, that during

the whole period of asphyxia the peripheral resistance is rising from

vaso-constriction. Under circumstances such as these, it is obvious

that _any_ heart must ultimately succumb, _no matter what anæsthetic is

in use_. It is also obvious that with chloroform and ethyl chloride,

which are themselves heart poisons, secondary syncope will happen much

more readily than with ether or nitrous oxide, which are not; and that

a heart with diseased musculature will fail quicker than a healthy

organ.

Secondary syncope is almost certainly the commonest fatal accident of

anæsthesia. The reason why this fact is not more widely recognised

arises from the natural instinct of any one who has suffered the misery

and ignominy of causing a death under an anæsthetic, to attribute it

to some cause beyond human control. The _essential_ cause of secondary

syncope is failure to maintain a free air way, which cannot be styled

unavoidable. Two consolations may, however, honestly be offered to the

person who has acted as anæsthetist in a case of secondary syncope.

Firstly, it is, in certain types of cases, very difficult indeed to

maintain a free air way; and secondly, a heart with muscle degenerated

from fatty or other changes, may give out after very little respiratory

embarrassment.

SYNCOPE FROM OVERDOSE.

This is a more gradual affair than the two foregoing; and has been

sufficiently dealt with in the chapter devoted to the Stages of

Anæsthesia (see p. 36).

C. REFLEX SYNCOPE.

Exceptionally, a patient not overdosed with anæsthetic, and not

suffering from any mechanical obstruction to respiration, has a sudden

attack of syncope during the progress of the operation. We here exclude

patients who are suffering from surgical shock; the condition arises

too rapidly for such an explanation to be accepted. Much speculation

has been expended upon these cases. One view is that some procedure of

the surgeon has set up a reflex inhibition of the heart through the

vagus; another, that the reflex has taken the form of sudden vasomotor

paresis. Levy would ascribe the condition to cardiac fibrillation.

It may well be that all cases cannot be met by one explanation. The

older surgeons stoutly maintained that reflex syncope could not arise

if the patient were properly under, and that it was in the practice

of those anæsthetists who were afraid of pushing the anæsthetic

sufficiently, that such accidents occurred. The author’s own belief

is that a _very_ light chloroform anæsthesia does pre-dispose to

this accident, but that it may occur also at a deep, the very deepest

possible level. With an anæsthetic other than chloroform, it is

extremely rare--perhaps unknown.

Treatment of Syncope.

This must be speedy to be of any avail. The following are the points

upon which to concentrate:--

(1) _Withdraw the anæsthetic._

(2) Make sure that the _air way is free_.

(3) Begin _artificial respiration_ by Sylvester’s method, the

movement of _expiration_ being first performed (_see_ Fig. 48).

(4) _Lowering of the head and shoulders_ is usually to be

recommended. It is best done by tilting the whole table as if

for the Trendelenberg position.

The lowering of the head attracts more blood to the carotid

artery and raises the blood pressure of the main vessel and

its cerebral branches (_see_ Fig. 35). It must, however, be

remembered that it will also tend to empty the blood in the

veins of the lower extremities and abdomen into the right side

of the heart, and cases in which marked cyanosis has preceded

pallor, are probably suffering already from engorgement and

dilatation of the right heart. The tilting of the table should

in such cases be very moderate in degree, and should not be

persisted in if it seems to do no good. In no case, indeed,

should the tilting be extreme. An angle of more than 15 or 20

degrees is as likely to do harm as good.

[Illustration: FIG. 48A.--Artificial respiration by

Sylvester’s method. Expiration.]

(5) Hot cloths may be placed over the precordial region, care

being taken not to burn the skin.

(6) The only _drugs_ likely to be of any avail are atropine and

strychnine, the former being used with the idea of paralysing

the terminations of the vagus in the heart muscle, the latter as

a cardiac tonic and a stimulant to the respiratory centre. Some

authorities have recommended the injection of atropine by a long

needle passed into the heart muscle, but most are content to

give either or both drugs hypodermically. Really to paralyse the

vagus, a very large dose of atropine is required--about ¹⁄₃₀ gr.

Strychnine should be given in a dose of ¹⁄₄₀–¹⁄₃₀ gr.

[Illustration: FIG. 48B.--Artificial respiration by

Sylvester’s method. Inspiration.]

(7) In cases where the right heart has certainly been

over-distended, the expedient of venesection has been tried.

Some six ounces may be withdrawn from the external jugular or

one of the veins of the arm.

(8) As a last resort, _the heart may be massaged_. The only

practicable route is to open the abdomen (if not already done)

pass one hand under the left side of the vault of the diaphragm,

placing the other hand over the precordial region. Between the

two hands, the heart can first be thoroughly compressed to empty

its presumably flaccid and over-distended cavities, and then

lightly massaged. Several cases of recovery from this measure

are on record.

Status Lymphaticus.

Before leaving the subject of accidents it may be well to allude

to this condition, which is also known as status thymicus, and as

lymphatism.

It is met with mostly in the young, the commonest ages probably being

five to fifteen years. Certain pathological conditions have been found

in fatal cases, of which the most important are an enlargement of the

thymus gland, of various lymph glands, and of the tonsils, including

the naso-pharyngeal tonsil (adenoids). The heart muscle is frequently

degenerated. Of the cause of these abnormalities we are as yet in

doubt. There is some reason to believe that the condition tends to

disappear with advancing years, if the subject survive.

The most outstanding clinical fact in connection with the disease

is its tendency to cause sudden death on very little provocation. A

fright, a sudden exertion, and above all an anæsthetic may cause sudden

and fatal syncope.

DIAGNOSIS.

Suspicion that the disease is present may be aroused in several ways.

The presence of enlarged tonsils and adenoids, combined with general

enlargement of lymph glands from no obvious cause, and a tendency

to faint, make a very suggestive picture. “Night-crowing” (a sudden

attack of laryngeal spasm, occurring at night, and often repeated

at intervals) also raises grave doubt. The diagnosis can only be

established with certainty by an X-ray photograph, when the great

enlargement of the thymus may be seen in the upper part of the chest.

ANÆSTHETICS IN STATUS LYMPHATICUS.

Too frequently the condition has never been suspected, and a fatality

occurs from sudden syncope, usually during the induction period, but

occasionally during the progress of the operation. It would, however,

be fallacious to suppose that an anæsthetic is necessarily fatal even

to an undoubted case. If the drug (preferably ether) be given with

great care, and the operation done carefully at a level of anæsthesia

neither too light nor too deep, there is every reason to believe that

the danger can be, and often is, successfully averted.

At the same time, it must be understood that in a known case, operation

should always be avoided or deferred if possible.

Handbook of anæsthetics · 第 16 / 21 章