While receiving supplemental O2 the first postoperative night, 28 of 32 patients maintained their SpO2 >90%, and none had an SpO2 nadir <85% (Figure 4). Breathing room air the second night, 18 patients (56%) experienced intermittent 5-min periods of hemoglobin desaturation with SpO2 nadirs <or=to90%; 11 patients (32%) experienced desaturation episodes of <85%, 7 patients (22%) experienced desaturation episodes of <or=to80%, and 3 patients (9%) experienced desaturation episodes of <or=to70%. chi squared analysis revealed significant differences (P < 0.05) between the two nightly SpO2 nadirs for each of the above designated levels, except the last.
No study patient died or sustained obvious permanent injury as a result of hypoxemia, but one patient had a major complication. She dosed herself relentlessly throughout the first postoperative night, receiving a total of 82 mg of morphine. She remained well oxygenated while breathing supplemental O2, but 45 min after her nasal O2 cannulae were removed the next morning, she was found to be almost comatose and deeply cyanotic. Her respiratory rate was 4 or 5 breaths/min, and she required assisted ventilation with a mask and self-inflating bag. She was given 1 mg of naloxone IV but remained sleepy, receiving O2 via a face mask until the following morning, when she began to ambulate without apparent untoward effect.
Hospital discharge of those patients who became hypoxemic was not delayed. The 18 patients with nocturnal SpO2 nadirs <or=to90% were discharged after 7.8 +/- 2.6 postoperative days, and those whose overnight SpO2 was >90% went home after 9.0 +/- 2.7 days. There was a poor correlation between individual nocturnal SpO2 nadirs and the number of days spent in hospital after surgery (r = -0.03).
SpO2 always fluctuated a little throughout both nights, and all patients exhibited intervals of minor hemoglobin desaturation at one time or another while using narcotic PCA. Some patients, however, sustained substantial nocturnal hypoxemia breathing room air, and to be able to identify those patients in advance would be of value. Thus, each patient's first night SpO2 nadir breathing with supplemental O2 was compared with their second night's SpO2 nadir breathing room air (Figure 5), and a good correlation was found (r = 0.64; P < 0.001). In fact, our study patients can be subdivided into three groups based on their nocturnal SpO2 nadir with O2 supplementation. In the seven patients who maintained their SpO2 >98% breathing supplemental O2, none became even mildly hypoxemic (SpO2 <90%) when exposed to room air. Of the 12 patients who achieved SpO2 nadirs of 95%-98% breathing nasal O2, 7 became mildly hypoxemic breathing room air, and 1 patient displayed severe hypoxemia (SpO2 <80%). Of the 13 patients with SpO2 nadirs <95% with nasal O2, 6 became severely hypoxemic the next night while breathing room air, and only 1 patient maintained an SpO2 >90%.
Most patients used PCA sporadically through the night, and there was an inconsistent temporal relationship between morphine self-administration and its effect on oxygenation. Some of the lowest SpO2 epochs occurred at the beginning of a several-hour period of frantic morphine self-administration, whereas others took place hours after dosing had ceased. Two of the four patients who took only 1 mg of morphine while breathing room air showed hemoglobin desaturation, and two of the seven patients who used PCA sparingly while receiving supplemental O2 still developed nocturnal SpO2 nadirs <90%. Nocturnal SpO2 nadirs breathing room air correlated poorly with age (r = -0.21), body mass index (r = -0.04), and the total dose of self-administered morphine (r = -0.22).
When postoperative pain is managed with PCA rather than by intermittent IM injection, patient satisfaction is high and narcotic consumption is reduced . No associated mortality or any permanent morbidity has ever resulted from properly delivered PCA. A few anecdotal incidents of excessive sedation or respiratory depression seem to be the only serious complications that have arisen [4-15]. Nevertheless, in this study, hypoxemia often developed overnight while patients attempted to control their own postoperative narcotic administration.
Narcotic analgesics decrease respiratory rate and minute volume. Hypoventilation results in carbon dioxide retention, and the ventilatory response to hypercapnia and hypoxemia are both reduced by narcotics [16,17]. Sleep itself is affected by narcotics in the postoperative period; rapid eye movement is nearly eliminated, and slow wave activity is severely suppressed . Sleep also becomes fitful and fragmented, and patients often display erratic breathing patterns [21-24]. These nocturnal episodes of abnormal ventilation are similar in character to those seen in individuals with sleep apnea; they, too, are accompanied by profound hypoxemia [22-24]. Providing supplemental O2 to patients after surgery improves oxygenation, but the narcotic-induced abnormal intervals persist [23,24], and their occurrence in the postoperative period far exceeds that of sleep apnea in the general population . Moreover, nocturnal hypoxemic episodes are rare in postoperative patients who receive continuous regional analgesia with local anesthetics . Nocturnal breathing patterns were not examined in our study, but we often observed SpO2 recordings with periods of significant hypoxemia (Figure 1, Figure 2, and Figure 3).
After surgery, patients experience discomfort, anxiety, and frequently periods of oppressive pain. Postoperative suffering stimulates ventilation and tends to counteract narcotic-induced respiratory depression . Indeed, the safety of PCA depends on the balance between these two opposite effects. Nevertheless, some patients develop significant narcotic-induced respiratory depression from PCA while still complaining of persistent, unrelieved pain . Others find deep breathing, coughing, and postoperative movement of any kind extremely painful. Their breathing becomes restricted and shallow, and narcotic therapy can actually improve ventilation [2,3]. Individuals vary greatly in their response to both postoperative pain and to opioids , and it is difficult to predict which patients treated with PCA will be susceptible to narcotic overdose.
In addition to modifying the pain threshold, narcotics cause dose-dependent drowsiness, mood changes, and mental clouding . If sedatives are prescribed in addition to narcotic PCA, respiratory depression is not uncommon after surgery [10,12,13]. The same sedated state is often induced in patients who use narcotic PCA alone. These patients act like inebriated individuals without inhibitions and without prudence. In fact, this behavior is not infrequently promoted by the hospital staff, who encourage patients to dose themselves liberally with their PCA devices at the first sign of discomfort and preemptively before bedtime.
Narcotic-induced hypoxemia is not a new or unexpected finding; it occurs with disturbing frequency when patients breathe room air in the postoperative period. SpO2 levels <or=to80% have often been reported in patients receiving IM narcotic injections after surgery on a PRN schedule [7,9,24,27,28]. Likewise, dangerous hemoglobin desaturation can develop in postoperative patients treated with continuous IV or epidural narcotic infusions [22,23,29-31]. The present study is the first to demonstrate a similar degree and incidence of hypoxemia in patients titrating their own narcotic administration via PCA.
Oxygen supplementation in operating theaters, in recovery rooms, in intensive care units, and during transport has become standard practice today for obtunded or recently sedated patients. Studies have repeatedly shown oxygen therapy to decrease postoperative hypoxemia in patients receiving narcotics by intermittent IM injections or by constant IV infusion [22-24,29,32]. Our study affirms the benefit of postoperative oxygen therapy when narcotics are administered at night via PCA devices. It remains to be determined whether hypoxemia is as severe in the daytime and for how long after surgery supplemental O2 is of value at night. This and another study have found benefit on the first two nights after hip surgery , and others have demonstrated narcotic-induced hypoxemia for 4 nights after other major operations [29,30,32]. However, O2 therapy can be uncomfortable, and its cost and that of PCA are issues that must be considered .
Central to our thesis, and still without definition, is the critical, life-threatening hypoxemic threshold [34,35]. However, when the PaO2 acutely decreases to <40 or 50 mm Hg and does not soon return to normal, central nervous system function declines, and some deficits persist . Adaptive physiologic modification also begins at that hypoxemic level: patients hyperventilate and compensatory cardiovascular mechanisms are initiated , erythropoietin synthesis increases , and tissues most sensitive to oxygen deprivation alter their genetic makeup so that vascularity increases . A substantial stress response is also elicited, and an increased incidence of myocardial ischemia has been reported after surgery in elderly patients who become severely hypoxemic [27,38,39]. Perhaps postoperative myocardial infarction occurs more frequently on surgical floors rather than in intensive care units because supplemental O2 is not routinely supplied there [40-42].
PCA-induced hypoxemia did not cause any patient permanent harm, but one patient did consume an inordinate amount of morphine overnight and required resuscitation. This near tragedy emphasizes the need to limit cumulative dosing over many hours. Perhaps patient monitors and alarms will one day be incorporated into a new generation of safer PCA devices, but until that time, we must recognize that individuals demonstrate large variation in their response to narcotics and to pain  and that ventilatory and cognitive function are not always affected equally [43,44].
We originally planned to study 100 patients, with each breathing room air one night and O2-supplemented air another. The O2 environment was to be randomly supplied the first night and reversed the next. However, when we examined our initial results, fear for patient safety dictated that we abandon randomization; consequently, the study conditions differed the two nights. Moreover, clinicians in our hospitals began to prescribe concurrent supplemental O2 with PCA whenever they suspected that their patients might develop hypoxemia; thus, our investigation ended prematurely. However, this small study has other serious weaknesses. No SpO (2) monitoring was performed in the preoperative period, and the possibility that these patients always become hypoxemic at night breathing room air cannot eliminated. We also lacked control groups who underwent the same monitoring but were treated with alternate acute pain therapies. Such patients may experience more or less hypoxemia. Moreover, this study does not address the possibility that surgical pain and suffering rather than narcotic administration may be the cause of the observed postoperative nocturnal hypoxemia.
Nevertheless, the extent of the hypoxemia that occurred in a high percentage of our patients who were breathing room air while using PCA is a remarkable and disturbing finding. PCA may be the safest mode yet devised for delivering narcotics, but we believe that our data suggest that both more careful monitoring and the provision of supplemental O2 should be considered whenever narcotic PCA is prescribed.
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