Anesthesiology THE SELECTION ADMINISTRATION
OF ANESTHETIC FOR DENTAL
HARRY M. SELDIN,
AGENTS AND THEIR OFFICE PROCEDURES
D.D.S., NEW YORK, N. Y.
HE history of anesthesia, as of any true science, is the history of ideas. Ideas are of value only if they embody fundamental truths. The fundamental truth is that Wells and Morton, both dentists, gave the art and science of anesthesia to humanity, and the history of the use of anesthesia is marked by the contributions of dentists. The record of the safe employment of general anesthesia in dent,istry is one that has yet to be equa1ed.l In spite of these facts, the right of dentists to use general anesthesia is now being threatened by certain medical groups. To avoid this threat, dentistry must clean its own house. In many dental offices general anesthesia is being administered by dentists or nurses who are not properly trained or qualified. In order, then, to insure the right of dentistry to continue to use general anesthesia, dentists must demonstrate their thorough knowledge of the modern concepts of anesthesiology, and their use of general anesthesia must constantly and in every way reflect this knowledge. Dentistry must also organize adequate graduate training and research centers in anesthesia in dental schools and in hospitals. The function of the anesthetist is to maintain t,hc patient in a satisfactory and safe anesthetic state. The anesthetist must st,rivc to disturb the normal physiology of the patient as little as possible, within the limitations imposed by the nature of the anesthetic state. This is accomplished by carrying the patient in the proper plane of anesthesia commensurate with the nature of the procedure being performed. The anesthetist must also consider the safety factor, which is determined solely by the physiologic condition of the patient while he is in the anesthetic state, regardless of the anesthetic level. Prior to the administration of any anesthetic agent, a preanesthetic evaluation must determine that the patient is able to withstand the stress of the anesthesia and surgery. The majority of these patients engage in normal and moderate physical activity. If the patient is able to go about his routine daily activities without experiencing or showing any symptoms of an inability to readily meet this stress, he can be considered to have an adequate cardiac reserve. Such a patient will
T
Presented
before
the
Boston
City
Hospital
Dental
156
Anesthesia
Society,
April
13, 1955.
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be able to withstand the stress of a properly chosen and well-administered general anesthetic. On the other hand, the patient who gives a history of shortness of breath or palpitation on exertion, swelling of the ankles, the need for two or For such a pamore pillows for sleeping, etc., may have a low cardiac reserve. tient a more thorough examination by a competent physician is advisable.
Choice of Anesthetic
Agent
In determining the choice of the anesthetic agent and technique, we must consider the fact that we are dealing in the dental office with ambulatory patients who arrive at the office just a short time prior to the beginning of the administration of the anesthetic. Unlike hospitalized patients, they expect to have the required dental surgery completed rapidly and painlessly and then to leave the office in a short time, free of the untoward or unpleasant effects which so often follow the administration of a general anesthetic. The ideal anesthetic agent for ambulatory patients should make possible’ (1) smooth, rapid, and pleasant induction, (2) easy maintenance, (3) rapid recovery, and (4) high safety factors. Since no single agent meets all these requirements, it becomes necessary to combine in use two or more agents to produce a balanced anesthesia. In balanced anesthesia we utilize and combine several drugs so that they supplement and complement each other to produce safer and more satisfactory anesthesia. Each drug should be selected for its specific effect. Thus, the combination of thiopental sodium with nitrous oxide-oxygen is employed to produce an ideal balanced anesthesia.
Nitrous Oxide.-For short procedures, such as extraction of one or several teeth or incision for drainage, nitrous oxide-oxygen administered by the rapidWith this technique, pure induction technique makes a pleasant anesthetic. nitrous oxide is administered until the first sign of light anesthesia becomes evident; adequate amounts of oxygen are then added. Thereafter, satisfactory anesthesia may be maintained with high percentages of oxygen in the anesthetic mixture. Supplements, such as Vinethene or trichloroethylene, may also be added to the mixture if necessary. The pendulum has again swung to nitrous oxide, for it is a true analgesic and anesthetic drug. It depresses the cerebral cortex without affecting either the cardiovascular or the respiratory centers, when used with sufficient oxygen during maintenance. In the absence of marked hypoxia, it causes the least postVagotonia with hypotension and bradycardia very anesthetic depression. rarely occur during light nitrous oxide-oxygen anesthesia. In anesthesia for oral surgery, the positive pressure, demand flow, fractional rebreathing machine is superior to other types. With this type of machine The we can obtain a faster and smoother induction and rapid denitrogenation. rapid elimination of nitrogen provides a higher concentration of oxygen and nitrous oxide in the alveoli. With rapid induction and denitrogenation, the patient can be maintained with 30 to 50 per cent oxygen in the anesthetic mixture.
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Intravenous Barbiturates.-Thiopental sodium (Pentothal sodium) and t.hiamylal sodium (Surital sodium) arc the two so-called “ultra short-acting” barbiturat,cs most c~ornmonly used at, prcscnt for office anesthesia. These drugs are metabolized in the body rather slowly; the t!erm “ultra short-acting” is consequently misleading. Thiopental is stored in the lipoid tissue and is passed back into the blood stream at a rat,e approximately equal to the rate at which it is detoxified in the b0dy.j Traces of the barbiturate have been found in the Hood stream many hours after administrat,ion. The patient should therefore not be allowed to leave the office alone, and certainly he should be cautioned against driving a car. Thiopental is primarily a hypnotic and does not produce a true analgesic state prior to the loss of consciousness. In anesthetic doses it depresses the respiratory center and thr cerebral cortex. With large doses of thiopental the threshold of hypoxic stimulation of th(‘ carotid body is raised and the sensitivity of the respiratory center to carbon dioxide stimulation is decreased. Although it is possible to produce and maintain anesthesia with the use of thiopental sodium alone,” without the use of any inhalation agent and without the use of oxygen, such a procedure is not in accord with the modern trends in anesthesia. Since thiopental sodium is a respiratory depressant, the patient does not, receive sufficient oxygen even for his decreased metabolism. Anoxic anoxia is conseyucnt,ly produced. McClure5 has demonstrated that barbiturates produce histotoxic hypoxia and that, even in therapeutic doses, they produce relatively severe hypoxia. In another study of anoxia in anesthesia, McClure and his associates” found that when thiopental sodium was employed for induction of anesthesia and nitrous oxide-oxygen in a ratio of 70:30 was used for maintenance, the arterial oxygen saturation remained normal or about normal. When, on the other hand, thiopental sodium was used as the sole anesthetic agent and the patient inhaled room air, the arterial blood oxygen saturation fell to as low as 69 per cent. Thiopental sodium, when administered too rapidly, may (*ause respiratory depression and cardiovascular decompensation.7 It is therefore very evident that the use of thiopental sodium for induction of anesthesia and nitrous oxide oxygen for maintenance produces a safer and more physiologic anesthesia. This provides what is undoubtedly the most satisfactory anesthesia obtainable for prolonged dental office procedures. With this technique, induction is rapid and pleasant. This combination induces overstimulated patients safely and easily and carries debilitated patients with safety. It produces a satisfactory anesthesia for all dental procedures with sufficient oxygen to prevent severe hypoxia. Recovery is relatively rapid, postanesthetic nausea is extremely rare, and the patient’s return to a normal physiologic state is hastened. We use thiopent,al sodium as a 2 per cent solution in normal saline solution, although it, may also bc used in distilled water or dextrose. A minimal dose (3 to 5 C.C.for the debilitated or aged and 10 to 15 cc. for the normal patient) is injected into a vein at a moderate pace. The eyeball usually rolls upward,
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the eyelid reflex is abolished, and unconsciousness ensues. Brief surgical procedures, lasting a minute or two, can then be performed without the addition of nitrous oxide-oxygen. Should the procedure last longer than one or two minutes, nitrous oxide-oxygen is added as soon as the lid reflex is abolished or the eyeball becomes eccentric. A minimum of 30 per cent oxygen is added, SO that the inhalation mixture contains 30 to 50 per cent oxygen and 50 to 70 per cent nitrous oxide. During prolonged surgery it may be advisable to add several cubic centimeters of thiopental sodium when the patient shows signs of too light anesthesia with this inhalation mixture. Should the thiopental sodium markedly depress the respirations, the anesthesia is too deep and more oxygen must be added. The anesthetist can assist the respirations by pressure on the With this technique, rebreathing bag or bellows in order to prevent acidosis. thiopental sodium is used as controlled premeditation to the nitrous oxide-oxygen. Thiopental sodium depresses the patient to the point where the nitrous oxide can be effective with relatively high oxygen percentages. Although the lid reflex and the eccentric fixation of the eyeball indicate light anesthesia, the clinical signs of the depth of thiopental sodium anesthesia The classic signs observable in nitrous oxideare of questionable reliability. oxygen anesthesia are not as evident during thiopental sodium anesthesia. The depth of anesthesia during thiopental sodium administration depends on the blood level of the drug. The initial dose, the total dose, the rapidity of injection, and the concentration of thiopental sodium influence the blood level. Thiopental sodium, in large enough doses, will result in respiratory depression. Premeditation with morphine or meperidine will produce profound respiratory depression, even in light thiopental sodium anesthesia. This depression is due primarily to the opiate or opiate-like drugs; the thiopental sodium simply enhances this depression. It is suggested, therefore, that opiates should not be used for premeditation. During the lighter stages of thiopental sodium anesthesia there is a hyperactivity of the laryngeal reflex; any stimulation may therefore produce a spasm or involuntary closure of the vocal cords, thus preventing gaseous exchange. With careful administration and management, such spasms are rare. Recent studies by Finks have shown that closure of the human larynx involves a dual mechanism consisting of a shutter and a ball valve. The shutter mechanism is formed by the vocal cords and is closed by the action of the cord adductor muscles, while the ball valve mechanism causes a closure by the extrinsic laryngeal muscles. Each mechanism can occur independently of the other. The shutter closure of the glottis causes an incomplete obstruction of the airway, resulting in a phonation or stridor. This stridor can occur during expiration or inspiration. The expiratory stridor occurs as a result of stimulus during light anesthesia. This spasm can be stopped by removing the stimulating cause or by deepening the anesthesia. The inspiratory shutter closure of the glottis occurs during the deeper planes of anesthesia and can be overcome by administering oxygen under pressure, thus lightening the plane of anesthesia.
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The obstruction callsed by the ball valve closure of the larynx is more There is an serious anti is caused by stimulation of the laryngeal mucosa. adduction of the vocal cords, which is followed by t,hr false cords. These spasms cannot bc broken by forcing oxygen under pressure. The proper treatment involves forcing t,he chin forward by pressure exerted behind the angles of the mandible; this tends to open the laryngeal airway. Aspirating blood and mucus in t,he area will tend to remove the stimulus causing the spasm. The additional administration of 2 to 4 cc. of thiopental sodium will deepen the plane of anesthesia and prevent recurrence of the spasm. If these measures fail, muscle relaxants must be resorted to. When this becomes necessary, 0.5 to 1 cc. of succinylcholine chloride (Anectine, Quelicin) will produce sufficient relaxation of the cords to break the spasm. When a muscular relaxant is being employed, it may be necessary to assist the respirations by pressure on the rebreathing bag or bellows. Special attention must be given to the pulmonary ventilation, especially during thiopental sodium anesthesia. Respiratory depression results in hypoxia and carbon dioxide retention. The combination of hypoxia and carbon dioxide retention is toxic to the cardiac mechanism and may cause cardiac arrest or ventricular fibrillation. In oral surgery, emphasis should be placed on the use of light anesthesia and adequate pulmonary ventilation to prevent respiratory acidosis. Considerable emphasis has been given to the use of chlorpromazine (Thorazine) for preoperative medication in anesthesia. A recent study by Weiss and associates” on t,he use of this drug for premeditation indicated that, chlorpromazine should not be used in preoperative medication in patients wit,11 extremes of blood pressure that is, under 100 mm. Hg systolic or above 160 mm. Hg systolic; patients with labile blood pressures; patients exhibiting jaundice, elevated serum bilirubin levels, or any evidence of liver disease; patients for whom a change to the head-up, prone, or lateral position is anticipated during surgery; and those extremely apprehensive patients for whom more profound sedation is necessary. Chlorpromazine may cause hypotension. The biliary emptying is frequently disturbed by this drug; this causes constipation and may also cause jaundice. The drug’s main value is its ability to reduce respiratory depression by reducing the amounts of narcotics that are administered. Chlorpromazine should not be used where epinephrine is given, as it may reverse its action. When injected subcutaneously, it may cause a severe tissue reaction, while a deep intramuscular injection of the drug may bc painful. In view of the fact that narcotic premeditation is seldom used in anesthesia for oral surgery procedures performed in the ofice, and in view of the fact that most oral surgery patients are seated in a head-up or supine position, the advisability of using chlorpromazine for premeditation in office anesthesia is questionable. In general, preoperative medication is no substitute for the sound application of psychologic techniques for emotional and apprehensive patients. We
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must remember that attached to the tooth is a human being who is undergoing Fright can what is to him an acutely threatening and emotional experience. manifest itself in different ways. Although tenseness, anxiety, and perspiration are the usual manifestations, other signs, such as depression, respiratory changes, and an unsolicited denial of fear, are also important. A few kind words of assurance and an explanation of what the patient is to experience during induction, told in a quiet, truthful manner, will eliminate most of the anxiety and fear and will also give the patient confidence in the anesthetist and surgeon.
Pregnant
Patients
Pregnancy, per se, is no contraindication for the administration of a general anesthetic. However, hypoxia and carbon dioxide retention must be aovided and cardiovascular distress must not be allowed to occur. Extreme caution should be exercised in administering general anesthesia in the first trimester of pregnancy. Traumatic stress and hypoxia could have a devastating effect on the developing embryo.
Management
of Children
To administer pediatric anesthesia successfully, the anesthetist should have a good understanding of the psychology of the child as well as the physiology and anatomy of his respiratory system. Young children have anatomic features that tend to interfere with an open airway. Their nervous control of respiration is not completely developed; thus, any interference with respiration will result in hypoxia. Prolonged hypoxia can be very dangerous to the child. This is especially true in children who have congenital cardiac anomalies or in anemic children. The prevention and early detection of hypoxia are of paramount importance. The parent should be given instructions on how to prepare the child for anesthesia. During induction, the child’s attention should be diverted by conversation, counting, or stories. Solid food, including milk, should not be given the child four to six hours preoperatively; tea with sugar or other sweet,ened clear fluids can be given orally up to two hours before surgery. Any anesthetic agent suitable for adults can be employed with safety for children, provided that constant attention is given to respiration and circulation. The unruly or apprehensive child can be managed successfully and with no psychologic trauma by the rectal administration of 1 to 4 C.C. of 10 per cent thiopental sodium (rectal) with anhydrous sodium carbonate as a buffer or of 10 per cent thiamylal sodium in normal saline. In the rest room, the child is told by the nurse that he is to have his temperature taken. A lubricated catheter, child’s size, is inserted into the rectum and the rectal thiopental sodium is administered. The child falls asleep in about fifteen minutes with the thiopental sodium and in about three minutes with the thiamylal sodium. He is then carried to the operating room, where the anesthesia is continued with nitrous
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oxide-oxygen. This premeditation with thiopental sodium or thiamylal sodium ( 13 mg. per pound of body weight) girts excclleni results. The dose is small, so that there is no recttd stimulation.
Management
of Aged
The aged need special consideration and care in the administration of anesthetics. The physical state of the aged patient about to be anesthetized must be evaluated. The percentage of healthy patients over 60 years of age is relatively small. The problem is not so much the patient’s age, as the morbid changes dut to cardiovascular, renal, and pulmonary disease. The choice of anesthetic and the method of administration should be based on the principle of providing the utmost safety for the patient. For the debilitated aged patient, local anesthesia is preferable to general anesthesia, wherever possible. Should a general anesthetic be indicated, 100 per cent oxygen is given for about one minute, followed by induction with thiopental sodium (4 to 8 cc. of 2 per cent solution) and maintenance with nitrous oxideoxygen 50-50. The patient is always kept in a light plane. This provides a safe general anesthetic for these patients. Deeper planes of anesthesia produce depression of the myocardium and vasomotor center. There is a fall in blood pressure, which may result in shock. The deeper the plane of anesthesia, the greater is the depression of t,he respiratory center. The normally healthy person can usually adjust to these changes in body physiology; the aged and poor-risk patient, however, cannot adjust so readily. These poor-risk patients must be carried in the very light plane with sufficient oxygen in the anesthetic mixture to maintain a high alveolar oxygen. IJpon completion of surgery, 100 per cent oxygen is administered for several minutes to wash out the nitrous oxide and supply a high oxygen concentration in the alveoli.
Treatment
of Emergencies
Accidental intra-arterial injection of thiopental sodium can be very serious and may result in loss of a finger and even a forearm. The immediate result of such an accident is intense arterial spasm, with possible trapping of some of the thiopental sodium. This produces an agonizing burning sensation and intense pain and blanching of the arm. The treatment is to assure vasodilatation and prevention of thrombosis. This can be accomplished by injecting procaine or lidocaine with 150 turbidity reducing units of hyaluronidase into the artery or area. The anesthetist must pay constant attention to respiration and pulse. As soon as any marked changes in respiration and pulse are noticed or the color becomes ashen gray and the pupils become dilated, resuscitative measures must be instituted to re-establish respiration and cardiac output. Oxygen under pressure, given through a tight face mask, should resuscitate the patient. If this fails, 0.25 to 0.5 cc. of l:l,OOO epinephrine diluted in 10 CC. normal saline or 4 to 5 C.C.of 2 per cent procaine is injected into the auricle; this injection is repeated in five minutes. Since cardiac arrest during anesthesia is more
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frequent in patients with heart disease than in those with normal hearts, a preanesthetic evaluation based upon an adequate history and examination is imperative in order to prevent cardiac arrest. All predisposing factors, such as apprehension, hypoxia, and hypercarbia, should be controlled and avoided if possible. In patients with known cardiac complications, the administration of 100 per cent oxygen for several minutes prior to the induction of anesthesia with thiopental sodium will make for greater safety. In surgical procedures about the head and neck, care must be taken to avoid the development of a carotid sinus reflex in order to avoid hypotension and bradycardia. Shock.-Shock should be treated with forced oxygen and intravenous glucose. Should these fail, the intravenous infusion of L-noradrenaline in a dose not exceeding 2 mg. will raise the blood pressure and produce recovery advises the intravenous infusion from seemingly irreversible shock. Lundy”’ of 500 cc. of 6 per cent solution of dextran in isotonic solution of sodium chloride containing 100 mg. of hydrocortisone. Hydrocortisone hemisuccinate reconstituted with 5 cc. of sterile physiologic saline, administered intravenously, can be lifesaving. This drug should always be available for emergency use. Where the vein is not obtainable, L-noradrenaline or Neosynephrine 5 mg. is combined with 150 turbidity reducing units of hyaluronidase and this combination is injected intramuscularly. The results of this injection are much slower than the results of the intravenous infusion. The administration of cortisone or hydrocortisone produces what is believed to be a reversible suppression of adrenal cortical function, and the use of corticotropin produces reversible adrenal hypertrophy. When the stress of general anesthesia and surgery is imposed upon patients in whom these pituitaryadrenal changes have occurred, the potential hazard of adrenal insufficiency becomes manifest. This may result in shock during or shortly after anesthesia and surgery if the patient was not properly prepared. This can be avoided by an adequate protective regimen given to these hormonally treated patients. As a preventive measure, all patients should be questioned as to whether they have conditions for which they are receiving or have recently been given any of these hormones. If such treatment is in progress, it is essential that it not be interrupted. Furthermore, if hormone therapy has been discontinued as recently as six months, adrenal insufficiency is possible and the patient should be referred to his physician for reinstitution of treatment with cortisone, hydrocortisone, or corticotropin before anesthesia is administered or surgery performed. Such hormone treatment must be continued for several days after Patients with possible adrenal insufficiency requiring emergency sursurgery. gery should be prepared with intravenous injection of 100 mg. lyophilized hydrocortisone (Solu-Cortef) dissolved in 2 C.C. of water. The patient should be continued on hormone therapy for several days postoperatively. Such procedures may be lifesaving. Conclusion Since more than 90 per cent of the oral surgeons in their offices, graduate training and research’centers
employ general anesthesia in anesthesia should be
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wtablishwl itI d011tal schools and in hospitals. ~:cncral anesthesia for dentistry must remain :m integral part of dental office practice and must be administered 1)~ or superviwd by dentists trained in the art and science of anesthesia. For short, procedures, nitrous oxide-oxygen anesthesia, maintained in the light, plane with ample oxygen in the mixture, is sound and safe. For prolonged surgical procedures in the office, induction with thiopental sodium and maintcnnnw with nitrous oxide-oxygen usin g a minimum of 30 per cent oxygen, provides the patient with a safe and pleasant anesthesia devoid of scvcrc hypoxia anti postancsthctic dcprcssion. Pregnant patients, young children, and the aged rccluire spc~4al consideration and management.
References 1. Seldin,
H. M., and Recant, I-1. 8.: Safety of Anesthesia in the Dsntal Office, d. Oral Surg. 199, 1955. 1-I. M.: Practical Anesthesia for Dental and Oral Surgery, ed. 3, Philadelphia, 1950, Lea & Fcbiger, p. 486. Fate of Thiopental in Man and a Method of Its Estimation Brodic, B. B., and others: in Biological Material, J. Pharmacol. & Exper. Therap. 98: 85, 1950. Krogh, H. W.: Intravenous Anesthesia in Office Practice, J. Oral Surg. 13: 138-148, 1955. McCluw, R. D., Hartman, F. W., Schnedorf, J. G., and Schelling, V. : Anoxia: Sourer of Possible Complications in Surgical Anesthesia, Ann. Surg. 110: 835, 1939. McClure, R. I)., Behrmann, V. G., and Hartman, F. W.: The Control of Anoxemia During Surgical Anesthesia With the Aid of Oxyhemagraph, Ann. Surg. 128: 685, 1948. Heller, M. L., Watson, R. W., and Storrs, R. C.: Analgesia With Nitrous Oxide-OxygenCurare for Major Surgery in the Poor-risk Patient, J. A. M. A. 161: X34-1542, 1956. Fink, B. R.: The Etiology and Treatment of Laryngeal Spasm, Anesthesiology 17: JulyAug., 1956. Weiss, W. A., McGee, J. I’., Jr., Bradford, J. O., and Hanks, E. C.: Value of Chlorpromazine in Preoperative Medication, J. A. M. A.. 161: 812, 1956. Lnndy, J. S.: Proc. Staff Meet., Mayo Clin. 30: 446-450, 1955. 13:
2. Seldin, 3. 4. 5. 6. 7. S. 9. 10.
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