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Apnea during spinal anesthesia in an unsedated patient with central sleep apnea syndrome
Case Reports Apnea During Spinal Anesthesia in an Unsedated Patient With Central Sleep Apnea Syndrome Saburo Tsujimoto, MD,* Chikara Tashiro, MD† Department of Anesthesiology, Hyogo College of Medicine, Nishinomiya City, 663-8501, Japan
We describe a case of apnea during spinal anesthesia in an unsedated patient with central sleep apnea syndrome. When spinal anesthesia is planned for a patient who is suspected of having this syndrome, apnea may be induced, even if no sedative was administered and the level of anesthesia is only moderate. © 2001 by Elsevier Science Inc. Keywords: Anesthesia, spinal; apnea: central sleep apnea syndrome, obstructive sleep apnea syndrome.
Introduction Central sleep apnea syndrome is a rarer syndrome than obstructive sleep apnea syndrome. There have been many reports on anesthetic management of the patient with obstructive sleep apnea, but there are few reports in the literature that describe the anesthetic management of a patient with central sleep apnea syndrome. To date, there has been no report of spinal anesthesia in such a patient. We report a case in which a patient showed frequent episodes of apnea and decreased oxygen saturation (SpO2) during spinal anesthesia in spite of a low anesthetic level and clear consciousness. Postoperative examination of this patient with an apnea monitor revealed central sleep apnea syndrome.
Case Report
*Assistant Professor †Professor of Anesthesiology Address correspondence to Dr. Tsujimoto at the Department of Anesthesiology, Hyogo College of Medicine, 1–1, Mukogawa-cho, Nishinomiya City, 663-8501, Japan. Received for publication October 4, 2000; revised manuscript accepted for publication March 5, 2001.
A slightly obese, 69-year-old man (body weight 84 kg, height 173 cm) was scheduled to undergo transurethral prostate resection (TURP) and prostate gland biopsy for prostatic tumor. He had a medical history of cerebral infarction and hypertension and had been treated with nicardipine and derapril [an angiotensin-converting enzyme (ACE) inhibitor]. There were no abnormal findings on preoperative electrocardiography (ECG) or respiratory function tests. Before arrival at the operating room, the patient was given no premedication, because he had requested a more detailed explanation of anesthesia. Electrocardiography, noninvasive blood pressure, SpO2, and capnography were monitored (HP Component Monitoring System, Hewlett-Packard, Hayward, CA). Capnograph was monitored by inserting a sampling tube into the nostril. On admission to the operating room, his blood pressure (BP) was 116/70
Journal of Clinical Anesthesia 13:309 –312, 2001 © 2001 Elsevier Science Inc. All rights reserved. 655 Avenue of the Americas, New York, NY 10010
0952-8180/01/$–see front matter PII S0952-8180(01)00263-X
Case Reports
Figure 1. Intraoperative trends as monitored by A. capnography and B. pulse oximetry. The capnograph shows a respiratory rate of 4 to 14 breaths per minute, and that the apneic episodes, the longest of which lasted 30 seconds, occurred once every 5 minutes. The capnograph was monitored by inserting a sampling tube into the nostril. SpO2 ⫽ oxygen saturation.
mmHg, heart rate (HR) 54 bpm, and SpO2 97%. Spinal anesthesia was placed at the L3-L4 interspace. Twelve milligrams (3 mL) of 0.4% high density tetracaine was administered in the subarachnoid space. One mg of etilefrine was administered 10 minutes after spinal anesthesia for hypotension and 30 minutes later 0.5 mg of atropine sulphate was administered for bradycardia. Thereafter, the patient showed stable hemodynamics. Although SpO2 was maintained between 94% and 99% within 30 minutes following spinal anesthesia, it decreased to less than 90% 3 to 4 minutes later. The decreased SpO2 was then restored to 100% by urging the patient to breathe deeply. Respiratory rate (RR) was 4 to 14 breaths/ min. An episode of apnea lasted as long as 30 seconds and was recognized once in 5 minutes (Figure 1). The frequency of apnea gradually decreased, there were no further episodes of decreased SpO2 noted 2 hours after spinal anesthesia. Although he closed his eyes most of the time during operation, the patient’s response to commands was prompt. He did not snore or display any other thoracoabdominal movement associated with respiratory efforts during apnea. Anesthesia levels measured by cold sign at the beginning and the end of the operation were Th10 and L1, respectively. At the end of the operation, the patient’s arterial blood gas analysis showed pH ⫽ 7.404; PaCO2 ⫽ 40.0 mmHg; PaO2 ⫽ 67.3 mmHg, and base excess ⫽ 0.3 mmol/L. On the tenth postoperative day, a screening test for sleep apnea syndrome was performed on the patient with the EdenTrace llTM (Nellcor-Puritan-Bennett, Minneapolis, MN). Frequent episodes of apnea, cessation of airflow 310
J. Clin. Anesth., vol. 13, June 2001
as a result of suspension of expiratory efforts, and decreases in SpO2, were observed when the patient was sleeping at night. Therefore, we suspected central sleep apnea syndrome (Figure 2).
Discussion In this case, paroxysmal apnea occurred frequently, and the patient was diagnosed with central sleep apnea syndrome. Central sleep apnea syndrome might have been induced by spinal anesthesia via the central nervous system (CNS), although the mechanism causing this occurrence is unknown. In the neural mechanism, which regulates respiration, there are two considerable control systems: voluntary adjustment and autonomous adjustment.1 The voluntary control system is located in the cerebral cortex, bypassing the respiratory center, and sending impulses to the respiratory motor neurons in the white matter of the spinal cord through the corticospinal tract. The autoregulatory control system is located in the pons and medulla oblongata, and sends impulses to the respiratory motor neurons. Central sleep apnea syndrome is a rarer syndrome than obstructive sleep apnea syndrome, and is generated by abnormalities in the respiratory center in the brainstem with no respiratory efforts needed.2 In a patient with central sleep apnea syndrome, apnea may develop when the patient sleeps, because respiration is mainly under abnormal autoregulatory control. Generally the effect of spinal anesthesia on respiration is only slight.3–5 But oversedation, high levels of spinal
Apnea during spinal anesthesia: Tsujimoto and Tashiro
Figure 2. Results of a screening test for sleep apnea syndrome with an apnea monitor (Eden-Trace II™, Nellcor-Puritan-Bennett, Minneapolis, MN). These waveforms were recorded from our patient during sleep on the tenth postoperative day. A. Normal breathing pattern with no apneic episodes observed. B. Abnormal breathing pattern showing an apneic episode while the patient was asleep. Cessation of airflow as a result of suspension of expiratory efforts and a decrease in oxygen saturation (SpO2) were observed. HR ⫽ heart rate.
anesthetic, and hypotension may often cause respiratory depression or respiratory arrest during spinal anesthesia. However, in this case, the patient had received no sedation, the anesthesia level was below Th10, and all hemodynamics, except transient hypotension and bradycardia, were stabilized early on during spinal anesthesia. Therefore, apnea could not have been caused by any of these factors. Even if sedative and analgesic drugs are not administered, hypoventilation and a decrease in SpO2 can occur in cases in which the spinal anesthesia works well. Although this mechanism is not clearly explained, a patient closes the eyes and seems to be sedated. Probably, the stimulation of the reticular activating system is reduced due to resolution of anxiety and afferent sensory nerve block. As a result, impulses to the respiratory center and the cerebral cortex may decrease, and central adjustment of respiration may be changed. Although we can’t rule out the possibility of other factors, the cause of apnea in this case might be explained by this hypothesis. As we mentioned above, there have been many reports
on anesthetic management for a patient with obstructive sleep apnea syndrome.6 On the other hand, there are few reports in the literature that concern anesthetic management of a patient with central sleep apnea syndrome.7 To date, there has been no report of spinal anesthesia in such a patient.
Conclusion When spinal anesthesia is planned for a patient who is suspected of having central sleep apnea syndrome, the apnea may be induced even if the anesthesia level is not very high. Careful respiratory monitoring using pulse oximetry and capnography should be done as such apneic episodes are impossible to prevent.
References 1. William FG: Review of Medical Physiology, 18th ed. Nowalk, CT: Appleton & Lange, 1997:679 – 81. J. Clin. Anesth., vol. 13, June 2001
311
Case Reports 2. Thalhofer S, Dorow P: Central sleep apnea. Respiration 1997;64: 2–9. 3. Steinbrook RA, Topulos GP, Concepcion M: Ventilatory responses to hypercapnia during tetracaine spinal anesthesia. J Clin Anesth 1988;1:75– 80. 4. Asklog VF, Smith PC, Eckenhoff JE: Changes in pulmonary ventilation during spinal anesthesia. Surg Gynecol Obstet 1984;119: 563–7.
312
J. Clin. Anesth., vol. 13, June 2001
5. Steinbrook RA, Concepcion M: Respiratory effects of spinal anesthesia: resting ventilation and single-breath CO2 response. Anesth Analg 1991;72:182– 6. 6. Boushra NN: Anaesthetic management of patients with sleep apnoea syndrome. Can J Anaesth 1996;43:599 – 616. 7. Wiesel S, Fox GS: Anaesthesia for a patient with central alveolar hypoventilation syndrome (Ondine’s Curse). Can J Anaesth 1990; 37:122– 6.
We describe a case of apnea during spinal anesthesia in an unsedated patient with central sleep apnea syndrome. When spinal anesthesia is planned for a patient who is suspected of having this syndrome, apnea may be induced, even if no sedative was administered and the level of anesthesia is only moderate. © 2001 by Elsevier Science Inc. Keywords: Anesthesia, spinal; apnea: central sleep apnea syndrome, obstructive sleep apnea syndrome.
Introduction Central sleep apnea syndrome is a rarer syndrome than obstructive sleep apnea syndrome. There have been many reports on anesthetic management of the patient with obstructive sleep apnea, but there are few reports in the literature that describe the anesthetic management of a patient with central sleep apnea syndrome. To date, there has been no report of spinal anesthesia in such a patient. We report a case in which a patient showed frequent episodes of apnea and decreased oxygen saturation (SpO2) during spinal anesthesia in spite of a low anesthetic level and clear consciousness. Postoperative examination of this patient with an apnea monitor revealed central sleep apnea syndrome.
Case Report
*Assistant Professor †Professor of Anesthesiology Address correspondence to Dr. Tsujimoto at the Department of Anesthesiology, Hyogo College of Medicine, 1–1, Mukogawa-cho, Nishinomiya City, 663-8501, Japan. Received for publication October 4, 2000; revised manuscript accepted for publication March 5, 2001.
A slightly obese, 69-year-old man (body weight 84 kg, height 173 cm) was scheduled to undergo transurethral prostate resection (TURP) and prostate gland biopsy for prostatic tumor. He had a medical history of cerebral infarction and hypertension and had been treated with nicardipine and derapril [an angiotensin-converting enzyme (ACE) inhibitor]. There were no abnormal findings on preoperative electrocardiography (ECG) or respiratory function tests. Before arrival at the operating room, the patient was given no premedication, because he had requested a more detailed explanation of anesthesia. Electrocardiography, noninvasive blood pressure, SpO2, and capnography were monitored (HP Component Monitoring System, Hewlett-Packard, Hayward, CA). Capnograph was monitored by inserting a sampling tube into the nostril. On admission to the operating room, his blood pressure (BP) was 116/70
Journal of Clinical Anesthesia 13:309 –312, 2001 © 2001 Elsevier Science Inc. All rights reserved. 655 Avenue of the Americas, New York, NY 10010
0952-8180/01/$–see front matter PII S0952-8180(01)00263-X
Case Reports
Figure 1. Intraoperative trends as monitored by A. capnography and B. pulse oximetry. The capnograph shows a respiratory rate of 4 to 14 breaths per minute, and that the apneic episodes, the longest of which lasted 30 seconds, occurred once every 5 minutes. The capnograph was monitored by inserting a sampling tube into the nostril. SpO2 ⫽ oxygen saturation.
mmHg, heart rate (HR) 54 bpm, and SpO2 97%. Spinal anesthesia was placed at the L3-L4 interspace. Twelve milligrams (3 mL) of 0.4% high density tetracaine was administered in the subarachnoid space. One mg of etilefrine was administered 10 minutes after spinal anesthesia for hypotension and 30 minutes later 0.5 mg of atropine sulphate was administered for bradycardia. Thereafter, the patient showed stable hemodynamics. Although SpO2 was maintained between 94% and 99% within 30 minutes following spinal anesthesia, it decreased to less than 90% 3 to 4 minutes later. The decreased SpO2 was then restored to 100% by urging the patient to breathe deeply. Respiratory rate (RR) was 4 to 14 breaths/ min. An episode of apnea lasted as long as 30 seconds and was recognized once in 5 minutes (Figure 1). The frequency of apnea gradually decreased, there were no further episodes of decreased SpO2 noted 2 hours after spinal anesthesia. Although he closed his eyes most of the time during operation, the patient’s response to commands was prompt. He did not snore or display any other thoracoabdominal movement associated with respiratory efforts during apnea. Anesthesia levels measured by cold sign at the beginning and the end of the operation were Th10 and L1, respectively. At the end of the operation, the patient’s arterial blood gas analysis showed pH ⫽ 7.404; PaCO2 ⫽ 40.0 mmHg; PaO2 ⫽ 67.3 mmHg, and base excess ⫽ 0.3 mmol/L. On the tenth postoperative day, a screening test for sleep apnea syndrome was performed on the patient with the EdenTrace llTM (Nellcor-Puritan-Bennett, Minneapolis, MN). Frequent episodes of apnea, cessation of airflow 310
J. Clin. Anesth., vol. 13, June 2001
as a result of suspension of expiratory efforts, and decreases in SpO2, were observed when the patient was sleeping at night. Therefore, we suspected central sleep apnea syndrome (Figure 2).
Discussion In this case, paroxysmal apnea occurred frequently, and the patient was diagnosed with central sleep apnea syndrome. Central sleep apnea syndrome might have been induced by spinal anesthesia via the central nervous system (CNS), although the mechanism causing this occurrence is unknown. In the neural mechanism, which regulates respiration, there are two considerable control systems: voluntary adjustment and autonomous adjustment.1 The voluntary control system is located in the cerebral cortex, bypassing the respiratory center, and sending impulses to the respiratory motor neurons in the white matter of the spinal cord through the corticospinal tract. The autoregulatory control system is located in the pons and medulla oblongata, and sends impulses to the respiratory motor neurons. Central sleep apnea syndrome is a rarer syndrome than obstructive sleep apnea syndrome, and is generated by abnormalities in the respiratory center in the brainstem with no respiratory efforts needed.2 In a patient with central sleep apnea syndrome, apnea may develop when the patient sleeps, because respiration is mainly under abnormal autoregulatory control. Generally the effect of spinal anesthesia on respiration is only slight.3–5 But oversedation, high levels of spinal
Apnea during spinal anesthesia: Tsujimoto and Tashiro
Figure 2. Results of a screening test for sleep apnea syndrome with an apnea monitor (Eden-Trace II™, Nellcor-Puritan-Bennett, Minneapolis, MN). These waveforms were recorded from our patient during sleep on the tenth postoperative day. A. Normal breathing pattern with no apneic episodes observed. B. Abnormal breathing pattern showing an apneic episode while the patient was asleep. Cessation of airflow as a result of suspension of expiratory efforts and a decrease in oxygen saturation (SpO2) were observed. HR ⫽ heart rate.
anesthetic, and hypotension may often cause respiratory depression or respiratory arrest during spinal anesthesia. However, in this case, the patient had received no sedation, the anesthesia level was below Th10, and all hemodynamics, except transient hypotension and bradycardia, were stabilized early on during spinal anesthesia. Therefore, apnea could not have been caused by any of these factors. Even if sedative and analgesic drugs are not administered, hypoventilation and a decrease in SpO2 can occur in cases in which the spinal anesthesia works well. Although this mechanism is not clearly explained, a patient closes the eyes and seems to be sedated. Probably, the stimulation of the reticular activating system is reduced due to resolution of anxiety and afferent sensory nerve block. As a result, impulses to the respiratory center and the cerebral cortex may decrease, and central adjustment of respiration may be changed. Although we can’t rule out the possibility of other factors, the cause of apnea in this case might be explained by this hypothesis. As we mentioned above, there have been many reports
on anesthetic management for a patient with obstructive sleep apnea syndrome.6 On the other hand, there are few reports in the literature that concern anesthetic management of a patient with central sleep apnea syndrome.7 To date, there has been no report of spinal anesthesia in such a patient.
Conclusion When spinal anesthesia is planned for a patient who is suspected of having central sleep apnea syndrome, the apnea may be induced even if the anesthesia level is not very high. Careful respiratory monitoring using pulse oximetry and capnography should be done as such apneic episodes are impossible to prevent.
References 1. William FG: Review of Medical Physiology, 18th ed. Nowalk, CT: Appleton & Lange, 1997:679 – 81. J. Clin. Anesth., vol. 13, June 2001
311
Case Reports 2. Thalhofer S, Dorow P: Central sleep apnea. Respiration 1997;64: 2–9. 3. Steinbrook RA, Topulos GP, Concepcion M: Ventilatory responses to hypercapnia during tetracaine spinal anesthesia. J Clin Anesth 1988;1:75– 80. 4. Asklog VF, Smith PC, Eckenhoff JE: Changes in pulmonary ventilation during spinal anesthesia. Surg Gynecol Obstet 1984;119: 563–7.
312
J. Clin. Anesth., vol. 13, June 2001
5. Steinbrook RA, Concepcion M: Respiratory effects of spinal anesthesia: resting ventilation and single-breath CO2 response. Anesth Analg 1991;72:182– 6. 6. Boushra NN: Anaesthetic management of patients with sleep apnoea syndrome. Can J Anaesth 1996;43:599 – 616. 7. Wiesel S, Fox GS: Anaesthesia for a patient with central alveolar hypoventilation syndrome (Ondine’s Curse). Can J Anaesth 1990; 37:122– 6.