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Pitfalls in nitrous oxide-oxygen anesthesia
PITFALLS HARRY
M.
IN NITROUS SELDIN,
OXIDE-OXYGEN
D.D.S.,
F.I.C.A.,
ANESTHESI,\
F.I.C.D.,
NEW
YORK,
N.
Y.
T
HE dentist who accepts general anesthesia as a requisite of the wider fields of oral surgery must, if he wishes to proceed with full confidence and control, accept also the fact that there are various pitfalls of anesthesia which may not only threaten its success but actually invoke disaster. These pitfalls are associated with types of patients other than the normal, and having learned to recognize these types, the anesthetist must know and observe the necessary precautions. Anoxemia must be considered as the most potential danger in nitrous oxide-oxygen administration. It is only through a thorough knowledge of the symptoms of anesthesia, and constant vigilance, that toxic anoxemia can be avoided. The Middle-Aged and the Elderly ll’ith Cardiocusculnr I)isenses.-With a middle-aged or elderly patient as the subject, the dent,ist must determine the patient’s ability to carry on the ordinary activities of daily routine. If he is capable of this, hc is a normal risk. On the other hand, if he is not, the reason should be ascertained. As a person advances in aqe, certain changes occur in the peripheral arteries, and sometimes even in the heart itself. Ordinarily he might lead a normal existence until something occurs to upset the pace-maker mechanism of the cardiovascular system. Any surgery might produce a certain amount of cardiac strain and therefore a patient suffering from high blood pressure, angina pectoris, or other cardiac lesion should be regarded as a cardiovascular hazard. Such patients, therefore, should always be maintained in the light plane of anesthesia. In an advanced degree of anoxemia there is a considerable washing-out of carbon dioxide, which is evidenced by a greyish color of the skin known as grey cyanosis. As a result of the elimination of this normal respiratory stimulant, there is a further increase of anoxemia. This vicious cycle may lead, in certain cardiac ailments, to a fall of systolic blood pressure, with resultant cardiovascular collapse ; or a marked rise in blood pressure leadin, (7 to cerebral hemorrhage and apoplexy. In such eventualities, intracardial injection of stimulating drugs such as adrenalin may be life-saving. Drugs affecting the peripheral vascular system, such as the hypodermic injection of caffeine-sodium-benzoate, or nitroglycerine administered under the tongue, often prove invaluable in restoring cardiac activity. Alcoholics.-Other types requiring special attention are the patients who admit, or give evidence of, alcoholic indulgence. Patient,s who imbibe heavily or consistently, require considerable care. They present difficulties, due to the changes in the blood vessels brought about by continued use of alcohol, which Institute.
Consulting Read
before
Oral the
Surgeon, Massachusetts
Harlem
Hospital, State
Dental 389
Nex Society.
York
City, Boston,
and Mass..
New April
York
City
15. 1941.
Cancer
390
IInrry M. Xeldin
This produces an hinder the free passage of oxygen from the blood to the cells. interference with the oxidation processes in the brain. Tluring induction they completely lose contact with t,heir outside environmcnt, become obstreperous, and are difficult to maintain in a smooth plane of anesthesia. They frequently pass quickly and suddenly from the excitement stage into the asphyxial stage of narcosis. Alcoholics should be premeditated with either 11/2 gr. nembutal, l/i gr. morphine, or 10 to 15 gr. of chloratone, as the drugs of choice. Dinbetics-It is unwise to anesthetize or operate on a known diabetic without the cooperation of his physician. It is imperative that such patients be under medical observation and cont,rol. If a diabetic is spilling sugar, he is on the verge of acidosis, and consequcnt,ly is very prone to asphyxia. lZnesthesia should not be attempted unless the urine is free from sugar, acetone, and diacetic acid, and t,hc blood sugar and carbon-dioxide combining power are within normal limits. Asphyxia superimposed on anesthesia will cause a rise in blood sugar; diabetic patient,s, therefore, should be carried in the light plane of anesthesia, and asphyxia should be avoided. Nitrous oxide and oxygen as an anesthetic do not affect the carbohydrate metabolism, and are therefore the general anesthetics of choice for the diabetic pat,ient. Nephriti~s.-~\cidosis is common in nephritics, and they are therefore sensitive to oxygen want. Xsph!rxia should be guarded against with these patients, as it might induce or incrcasc the acidosis. Nitrous oxide-oxygen anesthesia is particularly indicated in the presence of kidney disorders, as it is entirely eliminated through the lungs, placing no burden of escretion on the renal organs. Enzplz,t~scnttr (Bcr~el Chest) .-In the presence of emphysema (barrel chest) there is a dilat,ion of the pulmonary air vesicles, which is usually caused by the atrophy of the sept,a between the alveoli. The exchange of gases in the lungs of a pat,ient so afflicted is therefore interfered with, making him psrticularly susceptible to asphyxia. This type of patient should be kept light, as A marked increase in anoxemia may produce he does not tolerate oxygen want. an asphyxia which might prove fatal. Asthlrzrxtics.-Pat,ients afflict,ed with asthma usually suffer from some form of bronchial constriction. The passage of gases from the lungs to the blood is of the oxygen supply to the tisconsequently reduced, resultin, 0’ in a deficiency sues. Such patients, therefore, cannot tolerate acute asphyxia and must be carried in the light plane of anesthesia. Gnssed Patier&.--Patients who have lived through gas attacks during the past war, especially mustard gas, make trying subjects for gas-oxygen anesWar gases produce fibrotic changes in the lungs. thesia. The passage of gases such as oxygen, or an anesthetic, from the alveoli to the blood is consequently and maintenance of anesthesia interfered with, thus makin, v the induction difficult. It must be noted also, that once these patients arc saturated with the m asphyxia, resuscitation is slow and sometimes anesthetic to a point approachin, impossible, due to the obstruction of the passage of the gases from the alveoli to the tissues, and from the tissues back to the alveoli. Gassed patients sometimes offer no resistance to the anesthetic, taking it with much ease and in such quantities that they often slump, without warning, into the danger zone.
Nitrous
Oxide-Oxygen
Anesthesia
391
Pulmonary Atelectask--The development of pulmonary atelectasis, which is rather common following cpclopropane anesthesia, is not found as a postCyclopropane proanesthetic sequela with nitrous oxide-oxygen anesthesia. duces a slow, shallow and depressed respiration, thus also slowing down the circulation. The inefficient exchange of the alveolar gases favors the formation of atelectasis. Nitrous oxide anesthesia, on the other hand, produces a vigorous type of respiration. The lungs are in active movement, distending and collapsing regularly and rapidly, and producing an active circulation. The factors favoring atelectasis formation are therefore lacking. Patients ll’ith colds.-Dr. Rovenstein, Chief of the Department of Anesthesia at Bellevue Hospital, has made a study of upper respiratory infections and their effect on anesthesia. He found that patients with any upper respirat,ory infection, especially those with coughs from colds, produce a high percentage of postanesthetic lung complications and morbidity. Patients Slrturated With Pleonectic Dr?Lgs.-It is possible to tie up about one-third of the oxygen-carrying red cells with the use of pleonectie drugs, such as sulfanilamide, etc. These drugs combine with the hemoglobin! forming sulfhemoglobin, thus creating a form of anemic anoxemia. Such patients should be anesthetized in a manner similar to that employed for true anemic patients, namely, with the use of ample oxygen. Skull Fractures.--In injuries, with possible skull fractures, nitrous oxide should not be administered until the brain injury is fully diagnosed. Anoxemia in an already congested and injured brain might prove fatal. Anoxemia.-Carrying a patient in deep narcosis for a prolonged period produces cerebral anoxemia with either immediate or delayed aftermath. The nausea, headache, and depression sometimes experienced in gas oxygen anesthesia are usually due to prolonged anoxemia. When a patient awakens from an anesthetic and complains of numbness of either the feet or fingers, or shows spasmodic contractions, or clenches the thumb or fingers, or complains of persistent headaches or dizziness, or has severe crying spells, that patient has been carried too deep for too long a period, since these are all symptoms of anoxic anoxemia. In prolonged anesthesias, find, at intervals, the maximum oxygen percentage and carry the patient near that maximum. The longer a patient is asleep, the more oxygen he will require in the mixture. During nitrous oxide anesthesia, severe anoxemia may occur soon after induction or during prolonged maintenance. Fat.al anoxemic results, during primary anesthesia, usually occur in the overstimulated types, since the novice in anesthesia will tend to crowd the anesthetic in order to overcome the resistance offered by these patients. The warning symptoms of anoxemia are, however, very evident in such cases. In prolonged anesthesia fatal anoxemia may develop gradually and without warning; constant vigilance is therefore imperative in all prolonged cases. During prolonged anesthesia the symptoms may be confusing to the novice. If at all in doubt, a test should be made by administering 100 per cent oxygen
Hnm~ M. Seldin
392
for one to three inhalations. When a patient is too deep the resulting respirations after forced oxygen will be slow and shallow, or a period of apnea will follow. Should the patient show signs of wakefulness after this oxygen test, anoxemia was not present. CEREBRAI,
DAMAGE
DUE
TO
ANOXEMIB
IX
GSS
OXYGEN
ANESTHESIA
The extent of cerebral damage depends upon the duration and severity of anoxemia, or upon the duration of the respiratory and circulatory arrest. Nitrous oxide, if carried to a state of asphyxia, might produce several effects upon the patient: 1. Temporary injury to the brain. When the patient recovers from the anoxemic effect of nitrous oxide, within several hours to a day or two, and presents no residual effect of the cortex. 2. When the cerebral damage has been more severe, and t,he symptoms of asphyxia persist for several days, the patient may finally regain consciousness, but show symptoms of definite residual cortical damage, such as impairment in speech and rision or mental aspect. Such patients may never fully recover their mentality. 3. Where the cortical damage has been extensive, the patient may linger on from the depressing anoxemia due to nitrous oxide for several days and even weeks, wit,h marked convulsive muscular spasms, and later coma. When the brain degeneration finally becomes incompatible with life, the patient makes a delayed exodus. 4. Although in many instances of sudden death under nitrous oxide, some contributary factors can he found for the patient’s demise, there are cases where such death is due to asphyxia. In patients that linger on for three days or more, without regaining consciousness, and then finally succumb, there is usually evidence of frontal lobe affections of anoxic nature. Cortical and lenticular lesions are present upon aut,opsy, the superficial vessels of the brain are found to be extensively enlarged, the cortex is yellow, soft, and fragmented. There is a general disintegration of the cortex cells, the cells of Purkinje being damaged most seriously. Dr. Cyril B. Courville has shown that the destruction of the nerve cells. fibers, and lenticular nuclei of pa.tients who died from prolonged anoxemia of more than three days’ duration, are very similar to the damage produced experimentally on animals whose arteries, supplying the brain, are temporarily ligated, When a patient’s heart action has stopped thus producing severe anoxemia. for several minutes, and respirat,ion has stopped for more than ten minutes, cerebral damage due to anoxemia is a foregone conclusion. CARDIAC
FATI,URE
UNDER
GAS
OXYGEN
ASESTHESIA
Every now and then one reads or hears about a sudden death under nitrous oxide anesthesia. In a good many cases, the nitrous oxide was serving only as a coup de grace, the patient,‘s death bein, 0‘ due to some organic lesion such as coronary occlusion. Any exertion or excitement can serve as a contributing factor to break t,he thin thread of life in these patients.
Nitrous
Oxide-Oxygen
393
Anesthesia
Prolonged and severe anoxemia may so depress the cardiac centers in the medulla as to produce a sudden cardiac failure. However, certain factors, such as myocardial weakness, valvular lesions, and toxemia due to hyperthyroidism, favor cardiac failure. Since sudden death from nitrous oxide is caused by asphyxia, the patient should be examined for lesions that would predispose him to asphyxia. Cellulitis of the neck, peritonsillar or pharyngeal abscesses with edema extending into the larynx, greatly hinder respiration. Such patients should be carried under greater pressure and in the light plane of anesthesia. Carrying these patients in deep anesthesia, allowing blood and mucus to accumulate in the throat, the tongue to prolapse, or depressing the chin, will result in asphyxia with resultant depression of the respiratory and cardiac centers. In all sudden deaths under nitrous oxide, the classic changes in the gray matter of the brain are not present. The changes in the brain occur only in cases of prolonged anoxemia and where the patient survives more than fortyeight hours. The post-mortem findings in patients surviving less than fortyeight hours are those of acute pulmonary congestion and edema. Although nitrous oxide is the safest anesthetic for dental and oral surgery, it is not entirely devoid of danger. When administered by an anesthetist experienced with its use, it may be given with comparative safety, even to the poorest risk, provided he is kept in a light plane. The only danger with nitrous oxide is severe anoxemia, and if the patient is ma.intained in the light plane, toxic anoxemia can be avoided. REFERENCES Seldin, H. M.: Practical Anesthesia for Dental and Oral Surgery, 1934-41, Lea Hyman, Albert J.: Cardiac Emergencies in Dental Practice, New York J. Dent., Galbralth, E. S., and Steinberg, B.: Ann. Otol., September, 1937. Courville, C. FL: Untoward Effects of Nitrous Oxide Anesthesia, Pacific Press 1939.
& Febiger. March, 1939. Pub.
Assoc.,
M.
IN NITROUS SELDIN,
OXIDE-OXYGEN
D.D.S.,
F.I.C.A.,
ANESTHESI,\
F.I.C.D.,
NEW
YORK,
N.
Y.
T
HE dentist who accepts general anesthesia as a requisite of the wider fields of oral surgery must, if he wishes to proceed with full confidence and control, accept also the fact that there are various pitfalls of anesthesia which may not only threaten its success but actually invoke disaster. These pitfalls are associated with types of patients other than the normal, and having learned to recognize these types, the anesthetist must know and observe the necessary precautions. Anoxemia must be considered as the most potential danger in nitrous oxide-oxygen administration. It is only through a thorough knowledge of the symptoms of anesthesia, and constant vigilance, that toxic anoxemia can be avoided. The Middle-Aged and the Elderly ll’ith Cardiocusculnr I)isenses.-With a middle-aged or elderly patient as the subject, the dent,ist must determine the patient’s ability to carry on the ordinary activities of daily routine. If he is capable of this, hc is a normal risk. On the other hand, if he is not, the reason should be ascertained. As a person advances in aqe, certain changes occur in the peripheral arteries, and sometimes even in the heart itself. Ordinarily he might lead a normal existence until something occurs to upset the pace-maker mechanism of the cardiovascular system. Any surgery might produce a certain amount of cardiac strain and therefore a patient suffering from high blood pressure, angina pectoris, or other cardiac lesion should be regarded as a cardiovascular hazard. Such patients, therefore, should always be maintained in the light plane of anesthesia. In an advanced degree of anoxemia there is a considerable washing-out of carbon dioxide, which is evidenced by a greyish color of the skin known as grey cyanosis. As a result of the elimination of this normal respiratory stimulant, there is a further increase of anoxemia. This vicious cycle may lead, in certain cardiac ailments, to a fall of systolic blood pressure, with resultant cardiovascular collapse ; or a marked rise in blood pressure leadin, (7 to cerebral hemorrhage and apoplexy. In such eventualities, intracardial injection of stimulating drugs such as adrenalin may be life-saving. Drugs affecting the peripheral vascular system, such as the hypodermic injection of caffeine-sodium-benzoate, or nitroglycerine administered under the tongue, often prove invaluable in restoring cardiac activity. Alcoholics.-Other types requiring special attention are the patients who admit, or give evidence of, alcoholic indulgence. Patient,s who imbibe heavily or consistently, require considerable care. They present difficulties, due to the changes in the blood vessels brought about by continued use of alcohol, which Institute.
Consulting Read
before
Oral the
Surgeon, Massachusetts
Harlem
Hospital, State
Dental 389
Nex Society.
York
City, Boston,
and Mass..
New April
York
City
15. 1941.
Cancer
390
IInrry M. Xeldin
This produces an hinder the free passage of oxygen from the blood to the cells. interference with the oxidation processes in the brain. Tluring induction they completely lose contact with t,heir outside environmcnt, become obstreperous, and are difficult to maintain in a smooth plane of anesthesia. They frequently pass quickly and suddenly from the excitement stage into the asphyxial stage of narcosis. Alcoholics should be premeditated with either 11/2 gr. nembutal, l/i gr. morphine, or 10 to 15 gr. of chloratone, as the drugs of choice. Dinbetics-It is unwise to anesthetize or operate on a known diabetic without the cooperation of his physician. It is imperative that such patients be under medical observation and cont,rol. If a diabetic is spilling sugar, he is on the verge of acidosis, and consequcnt,ly is very prone to asphyxia. lZnesthesia should not be attempted unless the urine is free from sugar, acetone, and diacetic acid, and t,hc blood sugar and carbon-dioxide combining power are within normal limits. Asphyxia superimposed on anesthesia will cause a rise in blood sugar; diabetic patient,s, therefore, should be carried in the light plane of anesthesia, and asphyxia should be avoided. Nitrous oxide and oxygen as an anesthetic do not affect the carbohydrate metabolism, and are therefore the general anesthetics of choice for the diabetic pat,ient. Nephriti~s.-~\cidosis is common in nephritics, and they are therefore sensitive to oxygen want. Xsph!rxia should be guarded against with these patients, as it might induce or incrcasc the acidosis. Nitrous oxide-oxygen anesthesia is particularly indicated in the presence of kidney disorders, as it is entirely eliminated through the lungs, placing no burden of escretion on the renal organs. Enzplz,t~scnttr (Bcr~el Chest) .-In the presence of emphysema (barrel chest) there is a dilat,ion of the pulmonary air vesicles, which is usually caused by the atrophy of the sept,a between the alveoli. The exchange of gases in the lungs of a pat,ient so afflicted is therefore interfered with, making him psrticularly susceptible to asphyxia. This type of patient should be kept light, as A marked increase in anoxemia may produce he does not tolerate oxygen want. an asphyxia which might prove fatal. Asthlrzrxtics.-Pat,ients afflict,ed with asthma usually suffer from some form of bronchial constriction. The passage of gases from the lungs to the blood is of the oxygen supply to the tisconsequently reduced, resultin, 0’ in a deficiency sues. Such patients, therefore, cannot tolerate acute asphyxia and must be carried in the light plane of anesthesia. Gnssed Patier&.--Patients who have lived through gas attacks during the past war, especially mustard gas, make trying subjects for gas-oxygen anesWar gases produce fibrotic changes in the lungs. thesia. The passage of gases such as oxygen, or an anesthetic, from the alveoli to the blood is consequently and maintenance of anesthesia interfered with, thus makin, v the induction difficult. It must be noted also, that once these patients arc saturated with the m asphyxia, resuscitation is slow and sometimes anesthetic to a point approachin, impossible, due to the obstruction of the passage of the gases from the alveoli to the tissues, and from the tissues back to the alveoli. Gassed patients sometimes offer no resistance to the anesthetic, taking it with much ease and in such quantities that they often slump, without warning, into the danger zone.
Nitrous
Oxide-Oxygen
Anesthesia
391
Pulmonary Atelectask--The development of pulmonary atelectasis, which is rather common following cpclopropane anesthesia, is not found as a postCyclopropane proanesthetic sequela with nitrous oxide-oxygen anesthesia. duces a slow, shallow and depressed respiration, thus also slowing down the circulation. The inefficient exchange of the alveolar gases favors the formation of atelectasis. Nitrous oxide anesthesia, on the other hand, produces a vigorous type of respiration. The lungs are in active movement, distending and collapsing regularly and rapidly, and producing an active circulation. The factors favoring atelectasis formation are therefore lacking. Patients ll’ith colds.-Dr. Rovenstein, Chief of the Department of Anesthesia at Bellevue Hospital, has made a study of upper respiratory infections and their effect on anesthesia. He found that patients with any upper respirat,ory infection, especially those with coughs from colds, produce a high percentage of postanesthetic lung complications and morbidity. Patients Slrturated With Pleonectic Dr?Lgs.-It is possible to tie up about one-third of the oxygen-carrying red cells with the use of pleonectie drugs, such as sulfanilamide, etc. These drugs combine with the hemoglobin! forming sulfhemoglobin, thus creating a form of anemic anoxemia. Such patients should be anesthetized in a manner similar to that employed for true anemic patients, namely, with the use of ample oxygen. Skull Fractures.--In injuries, with possible skull fractures, nitrous oxide should not be administered until the brain injury is fully diagnosed. Anoxemia in an already congested and injured brain might prove fatal. Anoxemia.-Carrying a patient in deep narcosis for a prolonged period produces cerebral anoxemia with either immediate or delayed aftermath. The nausea, headache, and depression sometimes experienced in gas oxygen anesthesia are usually due to prolonged anoxemia. When a patient awakens from an anesthetic and complains of numbness of either the feet or fingers, or shows spasmodic contractions, or clenches the thumb or fingers, or complains of persistent headaches or dizziness, or has severe crying spells, that patient has been carried too deep for too long a period, since these are all symptoms of anoxic anoxemia. In prolonged anesthesias, find, at intervals, the maximum oxygen percentage and carry the patient near that maximum. The longer a patient is asleep, the more oxygen he will require in the mixture. During nitrous oxide anesthesia, severe anoxemia may occur soon after induction or during prolonged maintenance. Fat.al anoxemic results, during primary anesthesia, usually occur in the overstimulated types, since the novice in anesthesia will tend to crowd the anesthetic in order to overcome the resistance offered by these patients. The warning symptoms of anoxemia are, however, very evident in such cases. In prolonged anesthesia fatal anoxemia may develop gradually and without warning; constant vigilance is therefore imperative in all prolonged cases. During prolonged anesthesia the symptoms may be confusing to the novice. If at all in doubt, a test should be made by administering 100 per cent oxygen
Hnm~ M. Seldin
392
for one to three inhalations. When a patient is too deep the resulting respirations after forced oxygen will be slow and shallow, or a period of apnea will follow. Should the patient show signs of wakefulness after this oxygen test, anoxemia was not present. CEREBRAI,
DAMAGE
DUE
TO
ANOXEMIB
IX
GSS
OXYGEN
ANESTHESIA
The extent of cerebral damage depends upon the duration and severity of anoxemia, or upon the duration of the respiratory and circulatory arrest. Nitrous oxide, if carried to a state of asphyxia, might produce several effects upon the patient: 1. Temporary injury to the brain. When the patient recovers from the anoxemic effect of nitrous oxide, within several hours to a day or two, and presents no residual effect of the cortex. 2. When the cerebral damage has been more severe, and t,he symptoms of asphyxia persist for several days, the patient may finally regain consciousness, but show symptoms of definite residual cortical damage, such as impairment in speech and rision or mental aspect. Such patients may never fully recover their mentality. 3. Where the cortical damage has been extensive, the patient may linger on from the depressing anoxemia due to nitrous oxide for several days and even weeks, wit,h marked convulsive muscular spasms, and later coma. When the brain degeneration finally becomes incompatible with life, the patient makes a delayed exodus. 4. Although in many instances of sudden death under nitrous oxide, some contributary factors can he found for the patient’s demise, there are cases where such death is due to asphyxia. In patients that linger on for three days or more, without regaining consciousness, and then finally succumb, there is usually evidence of frontal lobe affections of anoxic nature. Cortical and lenticular lesions are present upon aut,opsy, the superficial vessels of the brain are found to be extensively enlarged, the cortex is yellow, soft, and fragmented. There is a general disintegration of the cortex cells, the cells of Purkinje being damaged most seriously. Dr. Cyril B. Courville has shown that the destruction of the nerve cells. fibers, and lenticular nuclei of pa.tients who died from prolonged anoxemia of more than three days’ duration, are very similar to the damage produced experimentally on animals whose arteries, supplying the brain, are temporarily ligated, When a patient’s heart action has stopped thus producing severe anoxemia. for several minutes, and respirat,ion has stopped for more than ten minutes, cerebral damage due to anoxemia is a foregone conclusion. CARDIAC
FATI,URE
UNDER
GAS
OXYGEN
ASESTHESIA
Every now and then one reads or hears about a sudden death under nitrous oxide anesthesia. In a good many cases, the nitrous oxide was serving only as a coup de grace, the patient,‘s death bein, 0‘ due to some organic lesion such as coronary occlusion. Any exertion or excitement can serve as a contributing factor to break t,he thin thread of life in these patients.
Nitrous
Oxide-Oxygen
393
Anesthesia
Prolonged and severe anoxemia may so depress the cardiac centers in the medulla as to produce a sudden cardiac failure. However, certain factors, such as myocardial weakness, valvular lesions, and toxemia due to hyperthyroidism, favor cardiac failure. Since sudden death from nitrous oxide is caused by asphyxia, the patient should be examined for lesions that would predispose him to asphyxia. Cellulitis of the neck, peritonsillar or pharyngeal abscesses with edema extending into the larynx, greatly hinder respiration. Such patients should be carried under greater pressure and in the light plane of anesthesia. Carrying these patients in deep anesthesia, allowing blood and mucus to accumulate in the throat, the tongue to prolapse, or depressing the chin, will result in asphyxia with resultant depression of the respiratory and cardiac centers. In all sudden deaths under nitrous oxide, the classic changes in the gray matter of the brain are not present. The changes in the brain occur only in cases of prolonged anoxemia and where the patient survives more than fortyeight hours. The post-mortem findings in patients surviving less than fortyeight hours are those of acute pulmonary congestion and edema. Although nitrous oxide is the safest anesthetic for dental and oral surgery, it is not entirely devoid of danger. When administered by an anesthetist experienced with its use, it may be given with comparative safety, even to the poorest risk, provided he is kept in a light plane. The only danger with nitrous oxide is severe anoxemia, and if the patient is ma.intained in the light plane, toxic anoxemia can be avoided. REFERENCES Seldin, H. M.: Practical Anesthesia for Dental and Oral Surgery, 1934-41, Lea Hyman, Albert J.: Cardiac Emergencies in Dental Practice, New York J. Dent., Galbralth, E. S., and Steinberg, B.: Ann. Otol., September, 1937. Courville, C. FL: Untoward Effects of Nitrous Oxide Anesthesia, Pacific Press 1939.
& Febiger. March, 1939. Pub.
Assoc.,