J Oral Maxillofac
Surg
48:942-944.1990
Incidence of Hypoxemia in the Postanesthetic Recovery Room in Patients Having Undergone Intravenous Sedation for Outpatient Oral Surgery JOHN H. HARDEMAN, DDS, MD,* STEPHEN R. SABOL, DDS,t AND MICHAEL S. GOLDWASSER, DDS, MD* This study prospectively quantitated the incidence of hypoxia in outpatients in a postanesthetic recovery unit following intravenous (IV) sedation. After identifying the high incidence of hypoxia by the use of pulse oximetry, supplemental oxygen was given to another group of patients and the incidence of the hypoxia was again monitored. Twenty of 100 patients experienced hypoxic episodes in the postanesthetic recovery unit when no supplemental oxygen was administered; only 3 of an additional 100 patients who received supplemental oxygen had episodes of hypoxia. The difference between the groups receiving and not receiving supplemental oxygen was both clinically and statistically significant. As result of this study, the use of supplemental oxygen is recommended for all patients undergoing IV sedation for outpatient oral surgery.
The patient undergoing intravenous (IV) sedation for outpatient oral and maxillofacial surgery is at risk for respiratory problems. Both benzodiazepines and narcotic analgesics depress the respiratory drive of the patient. Hypoxia and hypercapnea can result and reach unsafe levels within a few minutes, thus adversely affecting the expected anesthetic outcome. The respiratory effect may be even more profound and significant in the elderly, as well as in patients with underlying medical problems including chronic obstructive pulmonary disease and
obesity. The effects of hypoxemia and hypercarbia can impair perfusion of the cerebral arteries, initiate cardiac dysrhythmias, or even lead to cardiac arrest.’ Fortunately, the recent increase in intraoperative monitoring with electrocardiograms and pulse oximeters has allowed the surgeon or anesthesiologist to quickly detect the onset of hypoxia. After the diagnosis of respiratory depression, the problem may be corrected by adjusting the airway, administering supplemental oxygen, stimulating the patient, or by administering drugs to reverse the effects of the anesthestic agents. In the recovery room, however, many patients are subjected to conditions that are not well monitored, yet are conducive to the development of hypoxia. The residual anesthetic agents may cause continued depression of the respiratory drive.2 In a busy postanesthetic recovery room, when one nurse is responsible for the immediate postsurgical care, recovery, and discharge of patients, a few patients may not be monitored closely enough to detect and prevent possible hypoxia. It was the purpose of this study to prospectively quantitate the incidence of hypoxia in a postanesthetic recovery
* Resident in Oral and Maxillofacial Surgery, Carle Foundation Hospital, Urbana, IL. t Attending Surgeon, Oral and Maxillofacial Surgery Residency Program, Carle Foundation Hospital, Urbana, IL; Clinical Instructor, University of Illinois College of Medicine, UrbanaChampaign. $ Director of Oral and Maxillofacial Surgery Residency, Carle Foundation Hospital, Urbana, IL; Clinical Assistant Professor, University of Illinois College of Medicine, Urbana-Champaign. Address correspondence and reprint requests to Dr Hardeman: Carle Clinic Association, 602 W University Ave. Urbana, IL 61801.
0 1990 American geons
Association
of Oral and Maxillofacial
Sur-
0278-2391/90/4809-0006$3.00/O
942
HARDEMAN
943
ET AL
unit. For this study, significant hypoxia was defined as an oxygen desaturation of less than or equal to 90%.2 Methods One hundred patients who met the requirements of the American Society of Anesthesiologists (ASA) class I physical status and who were to undergo the surgical removal of four third molars under IV sedation/light general anesthesia were enrolled in this study. Perioperative parameters, such as age, weight, AS A status, duration of surgery, and type and amount of drug administered, as well as the time that each drug was administered, were recorded. Following surgery, the patients were wheeled to the recovery area and the initial postsurgical vital signs and management were performed. Each patient was then connected to a pulse oximeter and monitored during recovery. No supplemental oxygen was given, and the nursing staff was instructed to monitor each patient according to protocol. Patient response (asleep, awake, restless, and crying), oxygen saturation, and pulse were recorded every minute for the first 5 minutes and then every 5 minutes until 30 minutes had elapsed. The nursing staff was instructed to record the lowest oxygen saturation level during each period. At 30 minutes after surgery, most patients were ready to sit up and be redressed in preparation for discharge. Finally, the discharge status of the patient, including the patient’s response, oxygen saturation level, pulse, and blood pressure were recorded. After completion of the first phase of the study, another 100 ASA I patients were enrolled in the study. All parameters were exactly identical except all these patients received supplemental oxygen per nasal cannula at a flow rate of 3 L/min in the postanesthetic recovery unit. Again, the pulse oximeter was attached to the patient and the patients were monitored exactly as before. The ages of the 200 patients undergoing surgical removal of third molars under IV sedation ranged from 14 to 39 years. Eighty-three patients were male and 117 were female. The average duration of surgery was 34 minutes. The time of surgery began with the administration of the IV medications and ended with completion of the operation. The weight of the patients ranged from 45.5 kg to 104.5 kg. The standard dose of 100 pg of fentanyl was administered to each patient, which represented a range of 0.95 to 2.2 p,g/kg. Midazolam was given at the initiation of surgery and titrated to the desired clinical effect of slurred speech and lid ptosis. Total doses ranged from 0.1 mg/kg to 0.22 m&kg, with a mean of .16 mg/kg + .06 mg/kg. Methohexital was given to 9 of the patients, depending on the clinical effect of
the fentanyl and midazolam. Total dose in those patients receiving methohexital ranged from 0.36 to 6.5 mg/kg. None of the patients in the study received supplemental oxygen during surgery. Results During phase I of the study, in which the patients received no supplemental oxygen, 20 patients experienced hypoxic episodes while in the postanesthetic recovery room. There were two definite times at which the hypoxic events occurred. Ten patients developed hypoxia within the first 5 minutes in the recovery room. In the other 10, hypoxia occurred after the patient was in the recovery room for 10 minutes or longer. Several patients had more than one episode of hypoxia. Two patients had hypoxia in the first 5 minutes, returned to an oxygen saturation greater than 90%, and then became hypoxic again after 10 minutes of recovery room time. Additionally, one patient had a hypoxic episode that began at 3 minutes and lasted until after 15 minutes of recovery time despite both physical and verbal stimulation. During this time, she was noted to be sleeping, yet arousable. All the patients who experienced hypoxia had received lOO-p,gof fentanyl and a titrated dose of midazolam between 5 and 10 mg. Nine patients who received methohexital and 11 patients who did not receive methohexital became hypoxic. Of the patients experiencing hypoxic episodes, 12 were considered to be asleep, 7 were awake, and 1 was considered to be restless by the nursing staff. Of these patients who received supplemental oxygen, only three developed hypoxia. These patients received 100 kg of fentanyl and a titrated dose of midazolam. Two of the patients who became hypoxic received methohexital. All three developed hypoxia during the first 5 minutes of postanesthetic recovery. One patient had a single episode, whereas the other two had prolonged episodes of hypoxia. Most of the episodes occurred while the patients were asleep. One patient, however, like some of those in phase I, was considered to be awake, yet relaxed. All of the other patients in phase II maintained oxygen saturation greater than 90%. There was essentially no difference with regard to the dosage of medication administered to the 20 patients who developed hypoxia. The x2 analysis of these data showed the difference in hypoxic episodes between the two groups to be statistically significant (P = .OOl). Discussion This study documents the occurrence in the recovery room of arterial hypoxia in healthy patients
944
POSTANESTHETIC
who had undergone third molar removal under IV sedation as an outpatient. It also shows that supplemental oxygen in the postanesthetic recovery unit can be beneficial in decreasing the incidence of hypoxia. Among the patients who did not receive supplemental oxygen in the postanesthetic recovery unit, the frequency of hypoxia was significant; one fifth of the patients had one or more episodes of hypoxia. This showed that patients presumably without significant underlying pulmonary or cardiac problems can become hypoxic in the recovery room. Therefore, there is a need for the personnel caring for these patients to have a heightened awareness of this possibility. Furthermore, children, elderly, and medically compromised patients need particularly close attention because of the greater likelihood of becoming hypoxic.3 There are numerous factors contributing to postoperative hypoxia.4T5 Pulmonary secretions, postoperative bleeding, or the inability of the sedated patient to physically maintain an airway may cause a rapid decline in oxygen saturation of the blood. There is also a decreased respiratory drive in the postsedation patient and, of course, the respiratory depressant activity of midazolam, methohexital, and fentanyl are well known.336 The use of pulse oximetry is a necessary adjunct for monitoring to alert the surgeon or nurse of impending hypoxia. Indeed, cyanosis and the occurrence of dysrhythmias signify late and seriously low levels of oxygen saturation. ‘7’ The use of pulse oximetry in the evaluation of hypoxia has been shown to be very accurate in most settings.2*8,9 However, the pulse oximeter does have limitations. It does not directly measure arterial oxygen tension and therefore is subject to artifacts. Furthermore, the shape of the oxyhemoglobin dissociation curve allows for rapid decreases in arterial oxygen levels with only minor changes in the oxygen saturation below the 90% level (Fig 1).*JO Most pulse oximeters slightly overestimate arterial oxygen saturation when these levels are below the 70% leve1.8,9~” There have also been cases of false-normal oxygen saturation levels being indicated by the pulse oximeter.‘* Pulse oximeters are also susceptible to motion artifact, ambient light sources, dyes, venous pulsations, peripheral vasoconstriction, and hypotension. l3 Conclusion The results of this study show that there is a significant incidence of hypoxia in patients following
HYPOXEMIA
PO2(mm&d FIGURE curve.
1.
The normal
hemoglobin-oxygen
dissociation
IV sedation. This should be of concern to all oral and maxillofacial surgeons who use similar sedation techniques. The simple use of supplemental oxygen administered in the recovery room can significantly reduce the hypoxic episodes and avoid any related complications. References 1. Martin C: Pulmonary Physiology in Clinical Practice (ed 1). Boston, MA, Mosby, 1987, pp 112-128 2. Ehrenwerth J, Donielson D: Pulse oximetry in the postanesthetic care unit. J Post Anesth Nurs 2\9, 1987 _ 3. Miller RD: Anesthesia (ed 2). New York. NY. Churchill Livingstone, 1986 . ’ 4. Marshall BE, Wyche MG Jr: Hypoxema during and after anesthesia. Anesthesiology 37: 178, 1972 5. Craig DB: Postoperative recovery of pulmonary function. Anesth Analg 60:46, 1981 6. Catley DM, Thornton C, Jordan C, et al: Pronounced episodic oxygen desaturation in the postoperative period: Its association with ventilators patterns and analgesic regimen. Anesthesiology 63:20; 1985 7. Conroe JH. Botelino S: The Unreliabilitv of cvanosis in the recognition of arterial hypoxemia. Am J Med Sci 214:1, 1947 8. Yelderman M, New W: Evaluation of pulse oximetry. Anesthesiology 59:349, 1983 9. Brunel W, Cohen NH: Evaluation of the accuracy of pulse oximetry in critically ill patients. Crit Care Med 16:432, 1988 10. Guyton AC: Testbook of Medical Physiology (ed 7). Philadelphia, PA, Saunders, 1986 11. Severinghaus JW, Waifeh KH: Accuracy of six pulse oximeters to profound hypoxia. Anesthesiology 67551, 1987 12. Costarino AT, Davis DA, Deon TP: Falsely normal saturation readings with the pulse oximeter. Anesthesiology 67:830, 1987 13. Smith RA, Dodson TB, Cohen NH: Postoperative pulse oximetry in patients in maxillomandibular fixation. J Oral Maxillofac Surg 47:684, 1989
Surg
48:942-944.1990
Incidence of Hypoxemia in the Postanesthetic Recovery Room in Patients Having Undergone Intravenous Sedation for Outpatient Oral Surgery JOHN H. HARDEMAN, DDS, MD,* STEPHEN R. SABOL, DDS,t AND MICHAEL S. GOLDWASSER, DDS, MD* This study prospectively quantitated the incidence of hypoxia in outpatients in a postanesthetic recovery unit following intravenous (IV) sedation. After identifying the high incidence of hypoxia by the use of pulse oximetry, supplemental oxygen was given to another group of patients and the incidence of the hypoxia was again monitored. Twenty of 100 patients experienced hypoxic episodes in the postanesthetic recovery unit when no supplemental oxygen was administered; only 3 of an additional 100 patients who received supplemental oxygen had episodes of hypoxia. The difference between the groups receiving and not receiving supplemental oxygen was both clinically and statistically significant. As result of this study, the use of supplemental oxygen is recommended for all patients undergoing IV sedation for outpatient oral surgery.
The patient undergoing intravenous (IV) sedation for outpatient oral and maxillofacial surgery is at risk for respiratory problems. Both benzodiazepines and narcotic analgesics depress the respiratory drive of the patient. Hypoxia and hypercapnea can result and reach unsafe levels within a few minutes, thus adversely affecting the expected anesthetic outcome. The respiratory effect may be even more profound and significant in the elderly, as well as in patients with underlying medical problems including chronic obstructive pulmonary disease and
obesity. The effects of hypoxemia and hypercarbia can impair perfusion of the cerebral arteries, initiate cardiac dysrhythmias, or even lead to cardiac arrest.’ Fortunately, the recent increase in intraoperative monitoring with electrocardiograms and pulse oximeters has allowed the surgeon or anesthesiologist to quickly detect the onset of hypoxia. After the diagnosis of respiratory depression, the problem may be corrected by adjusting the airway, administering supplemental oxygen, stimulating the patient, or by administering drugs to reverse the effects of the anesthestic agents. In the recovery room, however, many patients are subjected to conditions that are not well monitored, yet are conducive to the development of hypoxia. The residual anesthetic agents may cause continued depression of the respiratory drive.2 In a busy postanesthetic recovery room, when one nurse is responsible for the immediate postsurgical care, recovery, and discharge of patients, a few patients may not be monitored closely enough to detect and prevent possible hypoxia. It was the purpose of this study to prospectively quantitate the incidence of hypoxia in a postanesthetic recovery
* Resident in Oral and Maxillofacial Surgery, Carle Foundation Hospital, Urbana, IL. t Attending Surgeon, Oral and Maxillofacial Surgery Residency Program, Carle Foundation Hospital, Urbana, IL; Clinical Instructor, University of Illinois College of Medicine, UrbanaChampaign. $ Director of Oral and Maxillofacial Surgery Residency, Carle Foundation Hospital, Urbana, IL; Clinical Assistant Professor, University of Illinois College of Medicine, Urbana-Champaign. Address correspondence and reprint requests to Dr Hardeman: Carle Clinic Association, 602 W University Ave. Urbana, IL 61801.
0 1990 American geons
Association
of Oral and Maxillofacial
Sur-
0278-2391/90/4809-0006$3.00/O
942
HARDEMAN
943
ET AL
unit. For this study, significant hypoxia was defined as an oxygen desaturation of less than or equal to 90%.2 Methods One hundred patients who met the requirements of the American Society of Anesthesiologists (ASA) class I physical status and who were to undergo the surgical removal of four third molars under IV sedation/light general anesthesia were enrolled in this study. Perioperative parameters, such as age, weight, AS A status, duration of surgery, and type and amount of drug administered, as well as the time that each drug was administered, were recorded. Following surgery, the patients were wheeled to the recovery area and the initial postsurgical vital signs and management were performed. Each patient was then connected to a pulse oximeter and monitored during recovery. No supplemental oxygen was given, and the nursing staff was instructed to monitor each patient according to protocol. Patient response (asleep, awake, restless, and crying), oxygen saturation, and pulse were recorded every minute for the first 5 minutes and then every 5 minutes until 30 minutes had elapsed. The nursing staff was instructed to record the lowest oxygen saturation level during each period. At 30 minutes after surgery, most patients were ready to sit up and be redressed in preparation for discharge. Finally, the discharge status of the patient, including the patient’s response, oxygen saturation level, pulse, and blood pressure were recorded. After completion of the first phase of the study, another 100 ASA I patients were enrolled in the study. All parameters were exactly identical except all these patients received supplemental oxygen per nasal cannula at a flow rate of 3 L/min in the postanesthetic recovery unit. Again, the pulse oximeter was attached to the patient and the patients were monitored exactly as before. The ages of the 200 patients undergoing surgical removal of third molars under IV sedation ranged from 14 to 39 years. Eighty-three patients were male and 117 were female. The average duration of surgery was 34 minutes. The time of surgery began with the administration of the IV medications and ended with completion of the operation. The weight of the patients ranged from 45.5 kg to 104.5 kg. The standard dose of 100 pg of fentanyl was administered to each patient, which represented a range of 0.95 to 2.2 p,g/kg. Midazolam was given at the initiation of surgery and titrated to the desired clinical effect of slurred speech and lid ptosis. Total doses ranged from 0.1 mg/kg to 0.22 m&kg, with a mean of .16 mg/kg + .06 mg/kg. Methohexital was given to 9 of the patients, depending on the clinical effect of
the fentanyl and midazolam. Total dose in those patients receiving methohexital ranged from 0.36 to 6.5 mg/kg. None of the patients in the study received supplemental oxygen during surgery. Results During phase I of the study, in which the patients received no supplemental oxygen, 20 patients experienced hypoxic episodes while in the postanesthetic recovery room. There were two definite times at which the hypoxic events occurred. Ten patients developed hypoxia within the first 5 minutes in the recovery room. In the other 10, hypoxia occurred after the patient was in the recovery room for 10 minutes or longer. Several patients had more than one episode of hypoxia. Two patients had hypoxia in the first 5 minutes, returned to an oxygen saturation greater than 90%, and then became hypoxic again after 10 minutes of recovery room time. Additionally, one patient had a hypoxic episode that began at 3 minutes and lasted until after 15 minutes of recovery time despite both physical and verbal stimulation. During this time, she was noted to be sleeping, yet arousable. All the patients who experienced hypoxia had received lOO-p,gof fentanyl and a titrated dose of midazolam between 5 and 10 mg. Nine patients who received methohexital and 11 patients who did not receive methohexital became hypoxic. Of the patients experiencing hypoxic episodes, 12 were considered to be asleep, 7 were awake, and 1 was considered to be restless by the nursing staff. Of these patients who received supplemental oxygen, only three developed hypoxia. These patients received 100 kg of fentanyl and a titrated dose of midazolam. Two of the patients who became hypoxic received methohexital. All three developed hypoxia during the first 5 minutes of postanesthetic recovery. One patient had a single episode, whereas the other two had prolonged episodes of hypoxia. Most of the episodes occurred while the patients were asleep. One patient, however, like some of those in phase I, was considered to be awake, yet relaxed. All of the other patients in phase II maintained oxygen saturation greater than 90%. There was essentially no difference with regard to the dosage of medication administered to the 20 patients who developed hypoxia. The x2 analysis of these data showed the difference in hypoxic episodes between the two groups to be statistically significant (P = .OOl). Discussion This study documents the occurrence in the recovery room of arterial hypoxia in healthy patients
944
POSTANESTHETIC
who had undergone third molar removal under IV sedation as an outpatient. It also shows that supplemental oxygen in the postanesthetic recovery unit can be beneficial in decreasing the incidence of hypoxia. Among the patients who did not receive supplemental oxygen in the postanesthetic recovery unit, the frequency of hypoxia was significant; one fifth of the patients had one or more episodes of hypoxia. This showed that patients presumably without significant underlying pulmonary or cardiac problems can become hypoxic in the recovery room. Therefore, there is a need for the personnel caring for these patients to have a heightened awareness of this possibility. Furthermore, children, elderly, and medically compromised patients need particularly close attention because of the greater likelihood of becoming hypoxic.3 There are numerous factors contributing to postoperative hypoxia.4T5 Pulmonary secretions, postoperative bleeding, or the inability of the sedated patient to physically maintain an airway may cause a rapid decline in oxygen saturation of the blood. There is also a decreased respiratory drive in the postsedation patient and, of course, the respiratory depressant activity of midazolam, methohexital, and fentanyl are well known.336 The use of pulse oximetry is a necessary adjunct for monitoring to alert the surgeon or nurse of impending hypoxia. Indeed, cyanosis and the occurrence of dysrhythmias signify late and seriously low levels of oxygen saturation. ‘7’ The use of pulse oximetry in the evaluation of hypoxia has been shown to be very accurate in most settings.2*8,9 However, the pulse oximeter does have limitations. It does not directly measure arterial oxygen tension and therefore is subject to artifacts. Furthermore, the shape of the oxyhemoglobin dissociation curve allows for rapid decreases in arterial oxygen levels with only minor changes in the oxygen saturation below the 90% level (Fig 1).*JO Most pulse oximeters slightly overestimate arterial oxygen saturation when these levels are below the 70% leve1.8,9~” There have also been cases of false-normal oxygen saturation levels being indicated by the pulse oximeter.‘* Pulse oximeters are also susceptible to motion artifact, ambient light sources, dyes, venous pulsations, peripheral vasoconstriction, and hypotension. l3 Conclusion The results of this study show that there is a significant incidence of hypoxia in patients following
HYPOXEMIA
PO2(mm&d FIGURE curve.
1.
The normal
hemoglobin-oxygen
dissociation
IV sedation. This should be of concern to all oral and maxillofacial surgeons who use similar sedation techniques. The simple use of supplemental oxygen administered in the recovery room can significantly reduce the hypoxic episodes and avoid any related complications. References 1. Martin C: Pulmonary Physiology in Clinical Practice (ed 1). Boston, MA, Mosby, 1987, pp 112-128 2. Ehrenwerth J, Donielson D: Pulse oximetry in the postanesthetic care unit. J Post Anesth Nurs 2\9, 1987 _ 3. Miller RD: Anesthesia (ed 2). New York. NY. Churchill Livingstone, 1986 . ’ 4. Marshall BE, Wyche MG Jr: Hypoxema during and after anesthesia. Anesthesiology 37: 178, 1972 5. Craig DB: Postoperative recovery of pulmonary function. Anesth Analg 60:46, 1981 6. Catley DM, Thornton C, Jordan C, et al: Pronounced episodic oxygen desaturation in the postoperative period: Its association with ventilators patterns and analgesic regimen. Anesthesiology 63:20; 1985 7. Conroe JH. Botelino S: The Unreliabilitv of cvanosis in the recognition of arterial hypoxemia. Am J Med Sci 214:1, 1947 8. Yelderman M, New W: Evaluation of pulse oximetry. Anesthesiology 59:349, 1983 9. Brunel W, Cohen NH: Evaluation of the accuracy of pulse oximetry in critically ill patients. Crit Care Med 16:432, 1988 10. Guyton AC: Testbook of Medical Physiology (ed 7). Philadelphia, PA, Saunders, 1986 11. Severinghaus JW, Waifeh KH: Accuracy of six pulse oximeters to profound hypoxia. Anesthesiology 67551, 1987 12. Costarino AT, Davis DA, Deon TP: Falsely normal saturation readings with the pulse oximeter. Anesthesiology 67:830, 1987 13. Smith RA, Dodson TB, Cohen NH: Postoperative pulse oximetry in patients in maxillomandibular fixation. J Oral Maxillofac Surg 47:684, 1989
