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Handbook of anæsthetics

Chapter 104: C. Reflex Syncope.
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About This Book

The handbook provides a concise practical guide to anaesthetic practice, beginning with physiological effects, shock, and asphyxia, then outlining methods of anaesthesia, patient preparation and clinical observation. Subsequent chapters review inhalational agents (nitrous oxide, ether, chloroform, ethyl chloride), gas mixtures and intratracheal techniques, inhaler and apparatus design, sequences of agents, and accident prevention and management. It addresses postoperative sequelae, patient positioning and criteria for choosing agents, and concludes with chapters on local and spinal anaesthesia. Emphasis is placed on safe administration, physiological monitoring, and practical details of equipment and technique.

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.

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.

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.