EPIDURAL AND INTRATHECAL OPIATES

Many clinical reports suggest that spinal (epidural or intrathecal) opiate administration may result in prolonged superior analgesia after surgery compared with parenteral administration in the traditional fashion (see Chapter 72 ). Moreover, clinical investigation has suggested that respiratory function, particularly after upper abdominal surgery,^[271] may be improved with epidural administration of morphine compared with intravenous administration. However, early reports of delayed respiratory depression after epidural and intrathecal morphine administration have led to scrutiny of the respiratory depressant effect of narcotics given by this route.^[272]

Several detailed clinical investigations of blood gases, ventilation, and respiratory drive have shown acceptable degrees of depression after spinal narcotic administration. However, assessment of the mean response in small numbers of individuals may not predict the likelihood of an extreme response, which may occur infrequently. Few large-scale surveys are available. Rawal and coworkers^[273] reported a survey of 93 departments of anesthesia in Sweden, in which during 1984 approximately 12,000 patients received epidural narcotics perioperatively, and 1000 patients received intrathecal narcotics. Most patients received morphine; 0.04% of patients showed clinical signs of ventilatory depression within 1 hour of epidural morphine injection, and 0.09% demonstrated delayed ventilatory depression. Delayed ventilatory depression occurred in 0.36% of patients who received intrathecal morphine. This occurred within 7 to 9 hours after injection. Stuart-Taylor and associates ^[274] reported that 7 of 800 patients receiving epidural diamorphine experienced respiratory depression to less than 10 breaths/min. Ready and colleagues^[275] reported that 2 of 1106 consecutive patients treated with epidural morphine after surgery required medication for respiratory depression. Scherer and coworkers^[276] reported that 1 of 1071 patients receiving thoracic epidural buprenorphine experienced respiratory depression. Lubenow^[277] reported six incidents of respiratory depression in 5172 patients receiving epidural narcotics. The incidence of respiratory depression after epidural analgesia is acceptably low for routine

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Although clinicians have tended to focus on the respiratory effects of epidural narcotics, respiratory depression and consequent hypoxemia can also occur after administration of narcotics by other routes. Periodic desaturation has also been reported after intravenous or intramuscular opiate administration.^{[79] [80] [85] [86] [89] [90] [92] [93] [286] [287] [288] [289] [290] [291]} One patient reported by Reeder^[89] after abdominal vascular surgery experienced 229 episodes of desaturation to SpO₂ less than 70%, representing 43% of the third postoperative night. Etches and associates ^[292] reported eight cases of serious respiratory depression out of approximately 1600 patients who had received intravenous opioids by means of patient-controlled infusion pumps. A comparative study demonstrated a higher incidence of respiratory depression among patients receiving narcotics by means of a patient-controlled infusion pump than with the epidural route.^[284] Subsets of patients who appear to be at higher risk for respiratory depression include the elderly^[293] and patients with a history of sleep apnea.^[294]

These observations suggest that narcotic administration through the epidural or intravenous routes carry a similar risk of mild or moderate episodic hypoxemia, although they have unknown clinical significance in most patients. Temporal association of transient hypoxemia with clinical events such as myocardial ischemia and confusion does not prove causation. Normal volunteers can be safely exposed to repetitive periods of hypoxemia (SaO₂ as low as 40%) for 30 to 45 seconds.^{[5] [141]} Although there is evidence that exposure to extreme hypoxia (mean lowest SaO₂ of 68%) for prolonged periods, along with hypocapnia, can cause minor psychomotor deficits,^[295] there is little evidence that exposure to moderate-alititude hypoxia for hours (e.g., for astronomers commuting daily from sea level to the Mauna Kea observatories at barometric pressure = 468 mm Hg, mean arterial PO₂ = 39.7 mm Hg and PCO₂ = 27.7 mm Hg)^[9] or even days results in permanent sequelae.^{[9] [296] [297]} In terms of assessing the risks of various forms of postoperative analgesia, mild postoperative reduction in SpO₂ is only a surrogate end point, which may not reflect the risk

TABLE 36-7 -- Frequency of respiratory rate and sedation monitoring following epidural analgesia in a survey of 197 institutions.

	Thoracic (N)		Lumbar (N)
Frequency	Continuous	Bolus	Continuous	Bolus
q1h	28	17	31	19
q1h × 24 hours, then q2h	25	14	27	17
q1h × 12 hours, then q2h	19	9	19	9
q1h × 4 hours, then q2h	12	3	13	5
q1h × 4 hours, then q4h	25	13	31	16
q2h	2	1	3	1
q2h × 24 hours, then q4h	9	1	9	1
q2h × 12 hours, then q4h	6	2	4	1
q4h	7	3	7	3
Totals	133	63	144	72
Data from Muir MR, Sullivan FL, Dear G, Ginsberg B: Monitoring practices following epidural analgesics for pain management: A follow-up survey. J Pain Symptom Manage 14:36, 1997.

of the most feared complication: major respiratory depression resulting in respiratory arrest or death.

Earlier reports recommended the routine use of apnea monitoring on patients given spinal narcotics, but apnea monitors are often associated with false alarms and are frequently ignored. Significant respiratory depression can occur with a normal respiratory rate.^{[192] [193] [195]} However, significant respiratory depression is almost invariably associated with sedation. A periodic check of mental status may be more sensitive than mechanical monitors in detecting clinical respiratory depression and is an essential component of monitoring patients who have received epidural narcotics.

Several years of clinical experience with epidural opiates have suggested that monitoring beyond clinical assessment is not necessary, particularly in low-risk patients,^{[195] [274] [275] [276] [277] [298] [299]} and have led to the implementation of less stringent policies in most institutions.^[300] Standards of care after epidural opioid administration in the United States were illustrated by a survey of 197 institutions, including teaching and community hospitals, published by Muir and colleagues.^[299] Patients were monitored in a general care ward after opioid administration through a thoracic epidural catheter in 88.6% of institutions and after lumbar administration in 96.8%. Pulse oximetry and electronic apnea monitoring were each routinely used in 28% of institutions after thoracic opioid administration, and in 27% and 5%, respectively, after lumbar administration. The frequency with which respiration rate and sedation are monitored is shown in Table 36-7 .

There is a fairly widespread consensus that monitoring equipment and resuscitative drugs should be readily available in addition to regular monitoring of respiration rate and level of sedation. Naloxone and a syringe with which to administer it should be available. Dosage adjustment or more intensive monitoring may be suitable for individuals with cardiorespiratory disease or other risk factors for respiratory depression ( Table 36-8 ). Because delayed respiratory depression can occur particularly after morphine administration, it is prudent to

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The widespread clinical use of epidural narcotics, particularly morphine, suggests that this technique is safe for most patients without the need for monitoring beyond simple clinical observation.