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.
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.
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.
(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.
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.