ANNUAL REVIEWS
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Copyright 1975. All rights reserved
Annu. Rev. Med. 1975.26:137-141. Downloaded from www.annualreviews.org Access provided by Syddansk University on 02/03/15. For personal use only.
KETAMINE ANESTHESIA
.7137
Charles F. Lanning, MD. and Merel H. Harmel, MD. Department of Anesthesiology, Duke University Medical Center, Durham, North Carolina 27710
Ketamine [2-(o-chlorophenyl)-2-methylamino cyclohexanone HCl], a unique gen eral anesthetic whose lack of cardiorespiratory depression is unequalled by any other general anesthetic currently available, was introduced in 1965 by McCarthy et al (1) and Domino, Chodoff & Corssen (2). It is an extremely versatile agent because it may be administered intravenously (Lv.) or intramuscularly (i.m.) without signifi cant tissue irritation. As yet, contraindications to its use with other drugs used in anesthesia have not been demonstrated. Ketamine provides a profound analgesia characterized by a trance-like, cataleptic state with generalized mild hypertonus, nystagmus, cardiovascular stimulation, lack of respiratory depression, and laryngeal and pharyngeal competence. Onset of action is rapid, being 20-30 sec for Lv. and 3-5 min for i.m administration. Duration of surgical anesthesia is 5-10 min and 15-25 min following i.v. and i.m. doses. The usual range of ketamine dosage is 1-2 mg/kg i.v. and 5-10 mg/kg i.m. Maintenance doses are usually one half the induc tion dose. Its use for outpatient procedures has progressively decreased because time-to-ambulation may be prolonged, frequently lasting more than 2 hr. Wessels, Allen & Slogoff (3) have demonstrated that NP enhances ketamine by reducing the total dose of ketamine 39% and shortening the recovery period by 64%. Initially, ketamine did not appear to provide visceral analgesia; but, its use with NP and relaxants provides adequate anesthesia for intraabdominal and thoracic surgery (4). For these reasons, ketamine is now more commonly used in combination with other anesthetic agents rather than as a monoanesthetic. Ketamine is rapidly distributed into all body tissues, primarily into fat, liver, lung, and brain. Metabolism occurs in the liver by N-demethylation and hydroxylation of the cyclohexanone ring with formation of water-soluble conjugates which are excreted in the urine. Human studies demonstrate an apparent biological half-life of 4 hr. with 70% urinary excretion in 24 hr. as the metabolized derivatives (5). However, Latarjet et al (6) have shown that ketamine's duration is not prolonged in humans with renal insufficiency. Ketamine has proved to have a broad therapeutic index. McCarthy et al (1) demonstrated in dogs a ketamine LDsoiEDso ratio five times that of pentobarbital. Repeated administrations have been given to humans without developing any sig137
Annu. Rev. Med. 1975.26:137-141. Downloaded from www.annualreviews.org Access provided by Syddansk University on 02/03/15. For personal use only.
138
LANNING & HARMEL
nificant tolerance or complication. Cumulation during anesthesia, however, does occur after multiple doses. Gross overdosage simply results in prolonged duration and respiratory depression. Postanesthetic anorexia (7) and immunosuppression (8), which are common to many general anesthetics, appear to be minimal with keta mine. The pharyngeal and laryngeal reflexes monoanesthetic. Preservation of these reflexes, incidence of laryngospasm, bronchospasm, and coughing secondary to secretions, blood, or manipulation in the oropharynx. These complications make ketamine a poor agent for endoscopy or oropharyngeal surgery. In addition, ketamine stimu lates marked salivation which must be blocked by an antisialagogue. Despite reten tion of protective reflexes, and, consequently, the airway must be safeguarded by one experienced in the management of airway obstruction and its complications. As with all general anes thetics, ketamine should be given with the usual precautions when a patient's stomach is full. Nevertheless, the degree of airway patency and lack of respiratory depression make ketamine the general anesthetic of choice when intubation is impossible. The decrease in airway resistance observed with ketamine makes it a desirable agent for bronchospastic and asthmatic patients (9). Although the mechanism of ketamine's cardiovascular stimulation is unknown, detailed studies demonstrate an increase in mean aortic pressure, pulmonary artery pressure, central venous pressure, heart rate, and cardiac index, and a variable effect upon peripheral vascular resistance (10, II). A summary of available information indicates that the adrenergic system must be intact in order for these responses to occur (12-14). Therefore, ketamine probably acts either directly by stimulating the central adrenergic centers or indirectly by inhibiting the neuronal uptake of cate cholamines, especially norepinephrine (15). These cardiostimulatory responses, in addition to its antiarrhythmic properties (I, 16), make ketamine a good induction agent for poor risk and hypovolemic patients. However, for maintenance, ketamine may be a liability in patients with severe coronary insufficiency since myocardial oxygen consumption has been shown to be elevated by ketamine (10). In addition, dogs made hypotensive by bleeding develop a greater oxygen debt and deteriorate earlier with ketamine than with halothane or neuroleptanalgesia (17). After bron chopulmonary lavage in man, one of us (CFL) has noted a greater base-deficit with ketamine-relaxant anesthesia than with halothane-relaxant anesthesia despite com parable acid-base status during lavage. The major deterrent to ketamine's wide acceptance has been the high incidence of postanesthetic emergence phenomena consisting of nausea, vomiting, restlessness, auditory and visual hallucinations, occasional frank delirium, and, especially, un pleasant dreams which have been reported to occur in 2-30% of patients (18, 19). Most of the dreams and hallucinatory phenomena may be related to misinterpreta tion of visual stimuli, resulting from nystagmus, and to a sense of bodily detachment which is probably created by a profound somatosensory analgesia. Although Hefez & Lanyi (20) have shown by reality testing that ketamine is not a psychotomimetic drug, the quality and content of the hallucinations and/or dreams may occasionally be compared to the reactions seen with common street hallucinogens.
Annu. Rev. Med. 1975.26:137-141. Downloaded from www.annualreviews.org Access provided by Syddansk University on 02/03/15. For personal use only.
KETAMINE ANESTHESIA
139
Emergence phenomena occur more frequently with a high dose per unit operative time; and, consequently, they are more frequent with short operative procedures. They are uncommonly reported in children. For this reason, ketamine is more often used in children than adults; especially, in uncooperative children when an intrave nous route is difficult to obtain. Emergence phenomena may be modified by narcot ics and/or tranquilizers given as premedication or prior to the end of anesthesia (21-25). It has also been suggested that they may be reduced by allowing a patient to recover undisturbed (26). This, however, creates a logistic problem in busy recovery rooms. The CNS effects of ketamine, as refel cted Corssen, Miyasaka, & Domino (26) as depression of the thalamo-neocortical system with activation of the limbic system. Because of this dual effect, they characterize ketamine as "dissociative anesthesia." Other authors (27-31), however, interpret the EEG changes solely as subclinical electroencephalographic seizure activity which they term "functional disorganization." For fear of creating frank convulsions, they recommend that ketamine be used with caution, if at all, in epileptic patients. In contrast, Corssen, Little & Tavakoli ( 32) found evidence to suggest that ketamine may have anticonvulsant properties and that it does not precipitate generalized convulsions in epileptic patients. Ketamine generates an increase in CSF pressure, particularly in patients with abnormal CSF flow crease may be attenuated by thiopental and controlled by induced hypocarbia. The effect upon the CSF appears to be directly related to an increase in cerebral blood flow produced by ketamine (34). In addition, cerebral oxygen consumption does not decrease as it does with other general anesthetics. Consequently, ketamine must be used with caution when a preexisting increase in CSF pressure is present. Ketamine produces a predictable, but slight, rise in intraocular pressure. Some feel this elevation is not sufficient to contraindicate the use of ketamine for patients with glaucoma (7, 35). However, its use with an open globe is not recommended. In patients for ocular surgery, ketamine-induced nystagmus may be controlled with very low doses of muscle relaxants. Providing no more than 2-3 mg/kg of ketamine is administered prior to umbilical cord clampage, significant newborn depression does not occur with vaginal or caesarean delivery ( 35, 36). With the limitations described, early fetal oxygenation and acid-base balance are unaltered ( 36, 37). An obstetrical advantage of ketamine is reduced uterine bleeding secondary to excellent postpartal uterine contractility ( 35, 38). Because of its long duration and the possibility of postanesthetic emergence phenomena, ketamine probably should not be used for spontaneous delivery; but, it may be beneficial for forceps delivery and obstetrical surgery such as in patients with placenta praevia. This objection to routine use may prove to be insignificant when ketamine is used in subanesthetic doses as recently described by Akamatsu et al (39). In summary, ketamine is a general anesthetic which is in its third and last stage of clinical development. Now, as with other anesthetics, its beneficial qualities/are being delineated and put to use for specific situations. Its major advantages are its
Annu. Rev. Med. 1975.26:137-141. Downloaded from www.annualreviews.org Access provided by Syddansk University on 02/03/15. For personal use only.
140
LANNING & HARMEL
ease of administration and rapid onset without cardiorespiratory depression, which make it particularly useful for poor risk patients and children. Ketamine's broad therapeutic index and lack of long term toxicity are indications for its use in situations such as repeated burn dressings and recurrent radiotherapy for uncooper ative children. Its cardiovascular stimulation makes it a good induction agent for debilitated and hypovolemic patients. Its respiratory benefits make it useful for asthmatic patients and for patients in whom spontaneous ventilation is imperative. It is particularly useful for cardiac catheterization where myocardial depression and positive pressure ventilation may markedly change pressure and shunt abnormali ties. Ketamine is contraindicated in those circumstances where hypertension might be detrimental such as in patients with a history, of cerebrovascular hemorrhage and intracranial, thoracic, and abdominal aneurysms. Marked hypertension may occur in patients receiving thyroxine medication (40). Corssen recommends that ketamine should not be used when systolic blood pressure is greater than 160 (26). This, however, is controversial because, in a hyper�ensive patient, hypotension may be even more detrimental than hypertension. Ketamine must be used with caution in patients with epilepsy or increased CSF pressure. It is not recommended for use in open globe eye surgery.
In conclusion, ketamine deserves a place in the anesthesiologist's armamentarium because of its many interesting features. However, future studies are needed to find means by which to control the major deterrents to its use; that is, postanesthetic emergence phenomena and ketamine-induced cardiovascular hyperreactivity. Literature Cited
I. McCarthy, D. A., Chen, G., Kaump, D. H., Ensor, C. 1965. J. New Drugs 5:21-33 2. Domino, E. F., Chodoff, P., Corssen, G. 1965. Clin. Pharmacol. Ther. 6:279-91 3. Wessels, 1. V., Allen, G. W., Slogoff, S. 1973. Anesthesiology 39:382-86 4. Vaughan, R. W., Stephen, C. R. 1974. Anesth. Analg. (Cleveland) 53:271-80 5. McCarthy, D. A., Glazko, A. J., Kurtz, S. June 18, 1970. Medical Summary Ketalar CI-581, 228-61. Ann Arbor, Michigan: Med. Sci. Aff. Div., Parke Davis 6. Latarjet, J. et al 1972. Anesth. Analg. Reanim. 29:261-64 7. Dillon, J. B. 1971. Proc. Roy. Soc. Med. 64:1153-56 8. Cullen, B. F., Chretien, P. B. 1973. Anesth. Analg. (Cleveland) 52:518-21 9. Corssen, G., Gutierrez, J.. Reves. J. G., Huber, F. C. Jr. 1972. Anesth. Analg. (Cleveland) 51 :588-96 10. Tweed, W. A., Minuck, M., Mymin, D. 1972. Anesthesiology 37:613-19
11. Virtue, R. W. et a1 1967. Anesthesiology 28:823-33 12. Chodoff, P. 1972. Anesth. Analg. (Cleveland) 51:247-50 13. Traber, D. L., Wilson, R. D., Priano, L. L. 1970. Anesth. Analg. (Cleveland) 49:420--26 14. Traber, D. L., Wilson, R. D. 1969. Anesth. Analg. (Cleveland) 48:248-52 15. Miletich, D. J., Ivankovic, A. D., Al brecht, R. F., Zahed, B., I1ahi, A. A. 1973. Anesthesiology 39:271-77 16. Dowdy, E. G., Kaya, K. 1968. Anes thesiology 29:931-43 17. Bruckner, J. B., Patschke, D., Rei necke, A., Tarnow, J. 1973. Anaes thesiol. Wiederbelebung 69:99-119 18. Albin, M. S., Dresner, A. J. June 18, 1970. Medical Summary Ketalar C/581, 142-59. Ann Arbor, Michigan: Med. Sci. Afr. Div.. Parke-Davis 19. Fine, J., Finestone, S. C. 1973. Anesth. Analg. (Cleveland) 52:428-30 20. Hefez, A., Lanyi, G. 1972. Isr. Ann. Psychiat. Relat. Disciplines 10:180--87
Annu. Rev. Med. 1975.26:137-141. Downloaded from www.annualreviews.org Access provided by Syddansk University on 02/03/15. For personal use only.
KETAMINE ANESTHESIA 21. Boville, J. G., Clarke, R. S. J., Dundee, J. W., Pandit, S. K., Moore, J. 1971. Brit. J. Anaesth. 43:600--8 22. Becsey, L., Malamed, S., Radnay, P., Foldes, F. F. 1972. Anesthesiology 37: 536-42 23. Sadove, M. S. et al 1971. Anesth. Analg. (Cleveland) 50:526-32 24. Collier, B. 1972. Anaesthesia 27:12()"':34 25. Rita, L., Seleny, F. L. 1974. Anesth. Analg. (Cleveland) 53:38()"':82 26. Corssen, G., Miyasaka, M., Domino, E. F. 1968. Anesth. Analg. (Cleveland) 47:746-59 27. Mori, K., Kawamata, M., Mitani, H., Yamazaki, y', Fujita, M. 1971. Anes thesiology 35:373-83 28. Kayama, K., Iwama, K. 1972. Anes thesiology 36:316-28 29. Winters, W. D., Ferrar-Allado, T., Guzman-Flores, C., Alcaraz, M. 1972. Neuropharmacology 11:303-15 30. Winters, W. D. 1972. Anesthesiology 36:309-12
141
31. Ferrer-Allado, T., Brechner, V. L., Dy mond, A., Gozen, H., Crandall, P. 1973. Anesthesiology 38:333-44 32. Corssen, G., Little, S. c., Tavakoli, M. 1974. Anesth. Analg. (Cleveland) 319-35 33. Shapiro, H. M., Wyte, S. R., Harris, A. B. 1972. Brit. J. Anaesth. 44:1200-4 34. Takeshita, H., Okuda, Y., Sari, A. 1972. Anesthesiology 36:69-75 35. Langrehr, D., Neuhaus, R. 1973. Acta Anaesthesiol. Belg. 24:71-96 36. Galbert, M. W., Gardner, A. E. 1973. Anesth. Analg. (Cleveland) 52:926-30 37. Levinson, G., Shnider, S. M., Gildea, J. E., deLorimier, A. A. 1973. Brit. J. Anaesth. 45:1111-15 38. Galloon, S. 1973. Can. Anaesth. Soc. J. 20:141-45 39. Akamatsu, T. J., Bonica, J. J., Rehmet, R., Eng, M., Ueland, K. 1974. Anesth. Analg. (Cleveland) 53:284-87 40. Kaplan,1. A., Cooperman, L. H. 1971. Anesthesiology 35:229-30
Further
Quick links to online content
Copyright 1975. All rights reserved
Annu. Rev. Med. 1975.26:137-141. Downloaded from www.annualreviews.org Access provided by Syddansk University on 02/03/15. For personal use only.
KETAMINE ANESTHESIA
.7137
Charles F. Lanning, MD. and Merel H. Harmel, MD. Department of Anesthesiology, Duke University Medical Center, Durham, North Carolina 27710
Ketamine [2-(o-chlorophenyl)-2-methylamino cyclohexanone HCl], a unique gen eral anesthetic whose lack of cardiorespiratory depression is unequalled by any other general anesthetic currently available, was introduced in 1965 by McCarthy et al (1) and Domino, Chodoff & Corssen (2). It is an extremely versatile agent because it may be administered intravenously (Lv.) or intramuscularly (i.m.) without signifi cant tissue irritation. As yet, contraindications to its use with other drugs used in anesthesia have not been demonstrated. Ketamine provides a profound analgesia characterized by a trance-like, cataleptic state with generalized mild hypertonus, nystagmus, cardiovascular stimulation, lack of respiratory depression, and laryngeal and pharyngeal competence. Onset of action is rapid, being 20-30 sec for Lv. and 3-5 min for i.m administration. Duration of surgical anesthesia is 5-10 min and 15-25 min following i.v. and i.m. doses. The usual range of ketamine dosage is 1-2 mg/kg i.v. and 5-10 mg/kg i.m. Maintenance doses are usually one half the induc tion dose. Its use for outpatient procedures has progressively decreased because time-to-ambulation may be prolonged, frequently lasting more than 2 hr. Wessels, Allen & Slogoff (3) have demonstrated that NP enhances ketamine by reducing the total dose of ketamine 39% and shortening the recovery period by 64%. Initially, ketamine did not appear to provide visceral analgesia; but, its use with NP and relaxants provides adequate anesthesia for intraabdominal and thoracic surgery (4). For these reasons, ketamine is now more commonly used in combination with other anesthetic agents rather than as a monoanesthetic. Ketamine is rapidly distributed into all body tissues, primarily into fat, liver, lung, and brain. Metabolism occurs in the liver by N-demethylation and hydroxylation of the cyclohexanone ring with formation of water-soluble conjugates which are excreted in the urine. Human studies demonstrate an apparent biological half-life of 4 hr. with 70% urinary excretion in 24 hr. as the metabolized derivatives (5). However, Latarjet et al (6) have shown that ketamine's duration is not prolonged in humans with renal insufficiency. Ketamine has proved to have a broad therapeutic index. McCarthy et al (1) demonstrated in dogs a ketamine LDsoiEDso ratio five times that of pentobarbital. Repeated administrations have been given to humans without developing any sig137
Annu. Rev. Med. 1975.26:137-141. Downloaded from www.annualreviews.org Access provided by Syddansk University on 02/03/15. For personal use only.
138
LANNING & HARMEL
nificant tolerance or complication. Cumulation during anesthesia, however, does occur after multiple doses. Gross overdosage simply results in prolonged duration and respiratory depression. Postanesthetic anorexia (7) and immunosuppression (8), which are common to many general anesthetics, appear to be minimal with keta mine. The pharyngeal and laryngeal reflexes monoanesthetic. Preservation of these reflexes, incidence of laryngospasm, bronchospasm, and coughing secondary to secretions, blood, or manipulation in the oropharynx. These complications make ketamine a poor agent for endoscopy or oropharyngeal surgery. In addition, ketamine stimu lates marked salivation which must be blocked by an antisialagogue. Despite reten tion of protective reflexes, and, consequently, the airway must be safeguarded by one experienced in the management of airway obstruction and its complications. As with all general anes thetics, ketamine should be given with the usual precautions when a patient's stomach is full. Nevertheless, the degree of airway patency and lack of respiratory depression make ketamine the general anesthetic of choice when intubation is impossible. The decrease in airway resistance observed with ketamine makes it a desirable agent for bronchospastic and asthmatic patients (9). Although the mechanism of ketamine's cardiovascular stimulation is unknown, detailed studies demonstrate an increase in mean aortic pressure, pulmonary artery pressure, central venous pressure, heart rate, and cardiac index, and a variable effect upon peripheral vascular resistance (10, II). A summary of available information indicates that the adrenergic system must be intact in order for these responses to occur (12-14). Therefore, ketamine probably acts either directly by stimulating the central adrenergic centers or indirectly by inhibiting the neuronal uptake of cate cholamines, especially norepinephrine (15). These cardiostimulatory responses, in addition to its antiarrhythmic properties (I, 16), make ketamine a good induction agent for poor risk and hypovolemic patients. However, for maintenance, ketamine may be a liability in patients with severe coronary insufficiency since myocardial oxygen consumption has been shown to be elevated by ketamine (10). In addition, dogs made hypotensive by bleeding develop a greater oxygen debt and deteriorate earlier with ketamine than with halothane or neuroleptanalgesia (17). After bron chopulmonary lavage in man, one of us (CFL) has noted a greater base-deficit with ketamine-relaxant anesthesia than with halothane-relaxant anesthesia despite com parable acid-base status during lavage. The major deterrent to ketamine's wide acceptance has been the high incidence of postanesthetic emergence phenomena consisting of nausea, vomiting, restlessness, auditory and visual hallucinations, occasional frank delirium, and, especially, un pleasant dreams which have been reported to occur in 2-30% of patients (18, 19). Most of the dreams and hallucinatory phenomena may be related to misinterpreta tion of visual stimuli, resulting from nystagmus, and to a sense of bodily detachment which is probably created by a profound somatosensory analgesia. Although Hefez & Lanyi (20) have shown by reality testing that ketamine is not a psychotomimetic drug, the quality and content of the hallucinations and/or dreams may occasionally be compared to the reactions seen with common street hallucinogens.
Annu. Rev. Med. 1975.26:137-141. Downloaded from www.annualreviews.org Access provided by Syddansk University on 02/03/15. For personal use only.
KETAMINE ANESTHESIA
139
Emergence phenomena occur more frequently with a high dose per unit operative time; and, consequently, they are more frequent with short operative procedures. They are uncommonly reported in children. For this reason, ketamine is more often used in children than adults; especially, in uncooperative children when an intrave nous route is difficult to obtain. Emergence phenomena may be modified by narcot ics and/or tranquilizers given as premedication or prior to the end of anesthesia (21-25). It has also been suggested that they may be reduced by allowing a patient to recover undisturbed (26). This, however, creates a logistic problem in busy recovery rooms. The CNS effects of ketamine, as refel cted Corssen, Miyasaka, & Domino (26) as depression of the thalamo-neocortical system with activation of the limbic system. Because of this dual effect, they characterize ketamine as "dissociative anesthesia." Other authors (27-31), however, interpret the EEG changes solely as subclinical electroencephalographic seizure activity which they term "functional disorganization." For fear of creating frank convulsions, they recommend that ketamine be used with caution, if at all, in epileptic patients. In contrast, Corssen, Little & Tavakoli ( 32) found evidence to suggest that ketamine may have anticonvulsant properties and that it does not precipitate generalized convulsions in epileptic patients. Ketamine generates an increase in CSF pressure, particularly in patients with abnormal CSF flow crease may be attenuated by thiopental and controlled by induced hypocarbia. The effect upon the CSF appears to be directly related to an increase in cerebral blood flow produced by ketamine (34). In addition, cerebral oxygen consumption does not decrease as it does with other general anesthetics. Consequently, ketamine must be used with caution when a preexisting increase in CSF pressure is present. Ketamine produces a predictable, but slight, rise in intraocular pressure. Some feel this elevation is not sufficient to contraindicate the use of ketamine for patients with glaucoma (7, 35). However, its use with an open globe is not recommended. In patients for ocular surgery, ketamine-induced nystagmus may be controlled with very low doses of muscle relaxants. Providing no more than 2-3 mg/kg of ketamine is administered prior to umbilical cord clampage, significant newborn depression does not occur with vaginal or caesarean delivery ( 35, 36). With the limitations described, early fetal oxygenation and acid-base balance are unaltered ( 36, 37). An obstetrical advantage of ketamine is reduced uterine bleeding secondary to excellent postpartal uterine contractility ( 35, 38). Because of its long duration and the possibility of postanesthetic emergence phenomena, ketamine probably should not be used for spontaneous delivery; but, it may be beneficial for forceps delivery and obstetrical surgery such as in patients with placenta praevia. This objection to routine use may prove to be insignificant when ketamine is used in subanesthetic doses as recently described by Akamatsu et al (39). In summary, ketamine is a general anesthetic which is in its third and last stage of clinical development. Now, as with other anesthetics, its beneficial qualities/are being delineated and put to use for specific situations. Its major advantages are its
Annu. Rev. Med. 1975.26:137-141. Downloaded from www.annualreviews.org Access provided by Syddansk University on 02/03/15. For personal use only.
140
LANNING & HARMEL
ease of administration and rapid onset without cardiorespiratory depression, which make it particularly useful for poor risk patients and children. Ketamine's broad therapeutic index and lack of long term toxicity are indications for its use in situations such as repeated burn dressings and recurrent radiotherapy for uncooper ative children. Its cardiovascular stimulation makes it a good induction agent for debilitated and hypovolemic patients. Its respiratory benefits make it useful for asthmatic patients and for patients in whom spontaneous ventilation is imperative. It is particularly useful for cardiac catheterization where myocardial depression and positive pressure ventilation may markedly change pressure and shunt abnormali ties. Ketamine is contraindicated in those circumstances where hypertension might be detrimental such as in patients with a history, of cerebrovascular hemorrhage and intracranial, thoracic, and abdominal aneurysms. Marked hypertension may occur in patients receiving thyroxine medication (40). Corssen recommends that ketamine should not be used when systolic blood pressure is greater than 160 (26). This, however, is controversial because, in a hyper�ensive patient, hypotension may be even more detrimental than hypertension. Ketamine must be used with caution in patients with epilepsy or increased CSF pressure. It is not recommended for use in open globe eye surgery.
In conclusion, ketamine deserves a place in the anesthesiologist's armamentarium because of its many interesting features. However, future studies are needed to find means by which to control the major deterrents to its use; that is, postanesthetic emergence phenomena and ketamine-induced cardiovascular hyperreactivity. Literature Cited
I. McCarthy, D. A., Chen, G., Kaump, D. H., Ensor, C. 1965. J. New Drugs 5:21-33 2. Domino, E. F., Chodoff, P., Corssen, G. 1965. Clin. Pharmacol. Ther. 6:279-91 3. Wessels, 1. V., Allen, G. W., Slogoff, S. 1973. Anesthesiology 39:382-86 4. Vaughan, R. W., Stephen, C. R. 1974. Anesth. Analg. (Cleveland) 53:271-80 5. McCarthy, D. A., Glazko, A. J., Kurtz, S. June 18, 1970. Medical Summary Ketalar CI-581, 228-61. Ann Arbor, Michigan: Med. Sci. Aff. Div., Parke Davis 6. Latarjet, J. et al 1972. Anesth. Analg. Reanim. 29:261-64 7. Dillon, J. B. 1971. Proc. Roy. Soc. Med. 64:1153-56 8. Cullen, B. F., Chretien, P. B. 1973. Anesth. Analg. (Cleveland) 52:518-21 9. Corssen, G., Gutierrez, J.. Reves. J. G., Huber, F. C. Jr. 1972. Anesth. Analg. (Cleveland) 51 :588-96 10. Tweed, W. A., Minuck, M., Mymin, D. 1972. Anesthesiology 37:613-19
11. Virtue, R. W. et a1 1967. Anesthesiology 28:823-33 12. Chodoff, P. 1972. Anesth. Analg. (Cleveland) 51:247-50 13. Traber, D. L., Wilson, R. D., Priano, L. L. 1970. Anesth. Analg. (Cleveland) 49:420--26 14. Traber, D. L., Wilson, R. D. 1969. Anesth. Analg. (Cleveland) 48:248-52 15. Miletich, D. J., Ivankovic, A. D., Al brecht, R. F., Zahed, B., I1ahi, A. A. 1973. Anesthesiology 39:271-77 16. Dowdy, E. G., Kaya, K. 1968. Anes thesiology 29:931-43 17. Bruckner, J. B., Patschke, D., Rei necke, A., Tarnow, J. 1973. Anaes thesiol. Wiederbelebung 69:99-119 18. Albin, M. S., Dresner, A. J. June 18, 1970. Medical Summary Ketalar C/581, 142-59. Ann Arbor, Michigan: Med. Sci. Afr. Div.. Parke-Davis 19. Fine, J., Finestone, S. C. 1973. Anesth. Analg. (Cleveland) 52:428-30 20. Hefez, A., Lanyi, G. 1972. Isr. Ann. Psychiat. Relat. Disciplines 10:180--87
Annu. Rev. Med. 1975.26:137-141. Downloaded from www.annualreviews.org Access provided by Syddansk University on 02/03/15. For personal use only.
KETAMINE ANESTHESIA 21. Boville, J. G., Clarke, R. S. J., Dundee, J. W., Pandit, S. K., Moore, J. 1971. Brit. J. Anaesth. 43:600--8 22. Becsey, L., Malamed, S., Radnay, P., Foldes, F. F. 1972. Anesthesiology 37: 536-42 23. Sadove, M. S. et al 1971. Anesth. Analg. (Cleveland) 50:526-32 24. Collier, B. 1972. Anaesthesia 27:12()"':34 25. Rita, L., Seleny, F. L. 1974. Anesth. Analg. (Cleveland) 53:38()"':82 26. Corssen, G., Miyasaka, M., Domino, E. F. 1968. Anesth. Analg. (Cleveland) 47:746-59 27. Mori, K., Kawamata, M., Mitani, H., Yamazaki, y', Fujita, M. 1971. Anes thesiology 35:373-83 28. Kayama, K., Iwama, K. 1972. Anes thesiology 36:316-28 29. Winters, W. D., Ferrar-Allado, T., Guzman-Flores, C., Alcaraz, M. 1972. Neuropharmacology 11:303-15 30. Winters, W. D. 1972. Anesthesiology 36:309-12
141
31. Ferrer-Allado, T., Brechner, V. L., Dy mond, A., Gozen, H., Crandall, P. 1973. Anesthesiology 38:333-44 32. Corssen, G., Little, S. c., Tavakoli, M. 1974. Anesth. Analg. (Cleveland) 319-35 33. Shapiro, H. M., Wyte, S. R., Harris, A. B. 1972. Brit. J. Anaesth. 44:1200-4 34. Takeshita, H., Okuda, Y., Sari, A. 1972. Anesthesiology 36:69-75 35. Langrehr, D., Neuhaus, R. 1973. Acta Anaesthesiol. Belg. 24:71-96 36. Galbert, M. W., Gardner, A. E. 1973. Anesth. Analg. (Cleveland) 52:926-30 37. Levinson, G., Shnider, S. M., Gildea, J. E., deLorimier, A. A. 1973. Brit. J. Anaesth. 45:1111-15 38. Galloon, S. 1973. Can. Anaesth. Soc. J. 20:141-45 39. Akamatsu, T. J., Bonica, J. J., Rehmet, R., Eng, M., Ueland, K. 1974. Anesth. Analg. (Cleveland) 53:284-87 40. Kaplan,1. A., Cooperman, L. H. 1971. Anesthesiology 35:229-30
