Respiratory Depression: Beyond the PACU, Before the ICUby Ashish K. Khanna, MD Volume 28 | Issue 1 | Winter 2017 Modern-day anesthesia is safe. Therefore, intraoperative mortality is rare. Unfortunately, the same cannot be said of postoperative mortality. Among a national sampling of inpatients who undergo surgery, 2% die within a month, with 50% of deaths occurring during the initial hospitalization.(1) If the 30 days after surgery were considered a disease, it would be the third leading cause of death in the United States.(2) Cardiorespiratory complications are by far the most common causes of 30-day postoperative mortality. Respiratory depression in the post-surgical period is common. The Agency for Healthcare Research and Quality (AHRQ) rated postoperative respiratory failure as the fourth most common patient safety event in its 2015 report, and the second most common if obstetric indicators were excluded. What constitutes respiratory depression? As simple as this may sound, there is no consensus on a true definition. A brief scan of the literature reveals that a combination of naloxone use, hypoventilation, hypercarbia, and hypoxemia, but utilizing varying durations and thresholds, has been used to define respiratory depression. The incidence of respiratory depression, based on these definitions, is ambiguous as well. In terms of numbers, the reported incidence varies from 0.1% to 41% depending on the defining criteria.(3) Where should we look for postoperative hypoxemia? The PACU and ICU are two destinations where patients frequently find themselves immediately after surgery. Though many clinicians feel that respiratory depression needs to be addressed most aggressively while in these care areas, I want to argue otherwise. The PACU and ICU are extensively monitored areas. Every vital sign is tracked continuously and every deviation from the norm results in a physician or nursing intervention. While residual anesthetic gases, muscle relaxants, and narcotics may be common offenders in the PACU, poor respiratory mechanics, baseline respiratory diseases, poor respiratory physiology, and secondary insults with ventilatory manifestations are big players for respiratory depression in the ICU. The bottom line is that we understand the reasons for respiratory impairment in these areas. Additionally, we know when it happens in real time. We can intervene, we can tackle specific causes, we can escalate care. It would stand to reason that patients rarely die of respiratory depression as an immediate and direct cause in the PACU and ICU. The road out of the PACU leads to the regular nursing floor. Generally, this is a place of comfort for clinically stable patients. Recently, our work with the VISION trial helped us to quantify hypoxemia on the surgical wards using blinded continuous saturation monitoring. We monitored continuous postoperative oxygen saturation in non-cardiac surgical patients for upto 48 hours after surgery. This monitoring started once the patient left the PACU or the ICU and reached the regular nursing floor. Importantly, bedside care providers were blinded to this oximetry. The nurses continued their routine checks on vital signs every four hours per protocol. The results told a story in themselves. Postoperative hypoxemia was common, serious, and prolonged. For example, 20% of patients demonstrated an average of 10 minutes of saturation <90% per hour over their entire hospitalization. And soberingly and rather shockingly, 90% of serious hypoxemic episodes (saturation <90% for ≥1 full hour) were completely missed by nurses conducting routine vital sign monitoring at four-hour intervals.(4) Patients continue to decompensate on the regular nursing floor, resulting in emergency medical team activation and transfer to higher levels of care. If repeated hypoxemic insults occur during these unmonitored periods, are we misplacing the emphasis in the respiratory depression story? Knowing how common the problem is, the next obvious question is whether we can better predict it. The answer unfortunately is no, at least not yet. While post-operative hypoxemia is common, it remains difficult to anticipate. We looked at a highly vulnerable population, that with obstructive sleep apnea. Surprisingly, STOP-BANG scores (a validated measure of obstructive sleep apnea risk) were not associated with the amount of postoperative oxygen desaturation.(5) Narcotics, which are often regarded as a common villain, take the blame for a lot of emergent floor to ICU transfers in the wee hours of the night. We examined the association of the type of narcotic (long- vs. short-acting) in patient controlled analgesia (PCA) systems and saw that the risk of hypoxemia was not reduced by using short-acting opioids.(6) Using commonly available information, it is not possible to reliably predict which postoperative inpatients will desaturate, or the severity of their hypoxemia. A recent closed claims analysis examined postoperative opioid induced respiratory depression.(7) Sadly, at least 77% of patients who had respiratory events suffered death or severe brain damage. As we suggested previously, only 9% had abnormal STOP-BANG scores. Importantly, 97% of these events were deemed preventable with better monitoring and response. Last but certainly not least,42% of these episodes occurred within 2 hours of the last nursing check.(7) So if postoperative respiratory depression is alarmingly common and we cannot predict it, can we do a better job of monitoring it? The question is a combination of how, what and who to monitor. Manually recorded oxygen saturation data were, on average, 6.5% higher than those recorded via automated systems in a large tertiary care medical center patient cohort.(8) While continuous pulse oximetry on the regular ward prevents ICU transfers and decreases rescue events, it is certainly not the be all and end all of respiratory monitoring.(9) The ASA recommends continuous monitoring of patients with neuraxial blocks and extended monitoring of those with obstructive sleep apnea. In addition, the guidelines from the ASA stress monitoring a combination of oxygenation and ventilation. The other important part to this puzzle is the heart, as respiratory events do not occur in isolation. Either tachycardia or hypoxemia may occur early on in a struggling patient, or the two may co-exist, and they often progress to hypotension, which is strongly associated with myocardial injury and death.(10, 11) As a corollary, it is well established that vital signs deteriorate 6–12 hours before cardiac and respiratory arrests occur(12-14) — which is the basis for having hospital rapid-response teams which undoubtedly save lives.(15) What is the solution to postoperative respiratory depression? A problem that causes a large number of surgical patients to be transferred from the floor to the ICU- sometimes once, sometimes repeatedly. A problem that for now lies somewhere in the corridor between the PACU and the ICU and knows no solution. The PRediction of Opioid-induced Respiratory Depression In Patients Monitored by capnoGraphY (PRODIGY) trial ClinicalTrials.gov Identifier: NCT02811302 may help answer some of those questions. For now, though, continuous automated cardiorespiratory monitoring appears to be the only real answer. A combination of oxygenation, ventilation and some minimum hemodynamic parameters should be monitored on everyone across the board. There are many more dimensions here to be explored. For instance, optimal handling of monitors and prevention of alarm fatigue are certainly important educational pieces for our colleagues on the regular nursing floors. As anesthesiologists and intensivists, we know respiratory depression too well. We also know that we cannot park everyone in the PACU or transfer everyone to the ICU. Beyond the confines of the PACU and before the doors of the ICU is the ‘grey area’ – an area that deserves better monitoring to prevent post-operative respiratory depression. Resources
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