Emergency Department Procedural Sedation with Propofol: Is it Safe?

Christopher S. Weaver, MD; * William E. Hauter, MD; *† Edward J. Brizendine, MS; ‡ William H. Cordell, MD*


J Emerg Med. 2007;33(4):355-361. 

In This Article


Propofol has many characteristics that make it attractive for emergency department procedural sedation. It induces rapid sedation and has an extremely short half-life, leaving the patient with no residual sedation soon after the procedure is over.[35] The safe use of propofol during EDPS is increasing.[1,2,3,4,5,6,7,8,9,10,11,12,13] Concern over the use of propofol for EDPS primarily surrounds the possibility of achieving a deeper-than-anticipated state of sedation and therefore encountering more serious complications. In our study, hypoxemia was the only sedation complication noted. However, the sedation complication of hypoxemia was brief and responded to simple airway maneuvers or increased oxygen concentration or delivery. No patient required advanced airway maneuvers such as intubation or even positive pressure ventilation. This may be due to the rapid recovery from propofol sedation.

Multiple studies demonstrate the safety of propofol in pediatric EDPS.[1,2,3] Each has identified a drop in blood pressure and transient hypoxemia as the most frequent complications. In all of the studies in which hypotension was identified there was no evidence of poor perfusion. The hypoxemia in all of these studies quickly responded to minimal intervention with no apparent lasting complications. Although these were pediatric studies, the results were very similar to ours in complication rates and sedation times. Our study did not demonstrate the frequency of decreased blood pressure seen in these pediatric studies but had similar hypoxemia rates.

In 2003, Miner et al. performed a randomized prospective study of adults undergoing EDPS for fracture or dislocation reduction.[4] They randomized patients to sedation with either propofol or methohexital. None of their patients had a significant drop in blood pressure. Respiratory depression occurred in 49% of the propofol group in their study and this was similar to the methohexital group. Two patients in the propofol group required bag-valve-mask as compared to four in the methohexital group. They defined respiratory depression as those developing hypoxemia (< 90%), absent ETCO2 waveform, and change in ETCO2 > 10 mm Hg. Although their study also demonstrated the safety of propofol in EDPS, our results identified a lower percentage of patients developing respiratory depression. In the Miner study, patients received a mean initial dose of 61 mg and a mean number of doses of 3.4. Our patients received a mean initial dose of 0.5 mg/kg (approximately 40 mg) and a mean number of doses of 3.9. It is possible that smaller, more frequent doses allow for titration of sedation while avoiding sedation complications. The patients with hypoxemia in the Miner study, as well as in our study, quickly responded to minimal, non-invasive interventions.

Taylor et al. compared propofol and midazolam/fentanyl for reduction of anterior shoulder dislocations.[5] They identified a respiratory depression rate of 22.9%. Each of their patients also responded to simple, non-invasive interventions. Our results suggest a lower rate of respiratory depression, although Taylor et al.'s definition of respiratory depression is not entirely clear. They did seem to have a similar rate of hypoxemia to our results. Taylor and colleagues used a higher initial dose (1.5 mg/kg vs. 0.5 mg/kg) and fewer total doses than the doses utilized in our study. As discussed above, the difference in dosing may contribute to the higher level of respiratory depression, if it indeed exists.

Burton et al. reported a prospective, descriptive series of patients receiving propofol for EDPS at three study sites.[6] The frequency of events was consistent across the three sites. They identified hypoxemia as the most frequent complication with an occurrence rate of 7.7%. Their findings were consistent with our results, with a slightly lower hypoxemia rate as compared to the 11% in this study; 3.9% of their patients received bag-valve mask ventilation whereas none of our smaller series required this treatment. Their mean initial dose of propofol was 1.2 mg/kg with a mean total dose of 3.6 mg/kg as compared to our initial dose of 0.5 mg/kg and mean total dose of approximately 1.5 mg/kg.

Swanson et al. demonstrated the safety of propofol when used as a continuous infusion with a similarly small number of complications, as seen in our results.[7] Other articles have reported the safety of propofol in EDPS while studying various parameters such as ETCO2 monitoring, bispectral index monitoring, and EDPS in critically ill patients.[8,9,10,11] Each study identifies respiratory depression and transient hypoxemia as the most frequent complications associated with EDPS with propofol and demonstrate rates similar to those seen in EDPS with other agents in the same studies. The results of these studies are similar to the Miner et al. study referenced in the paragraph above.[4]

We saw no evidence of aspiration in any of the patients undergoing EDPS with propofol despite the high incidence of so-called "NPO violations." It should be noted that the individual emergency physician was responsible for the decision to sedate a patient despite NPO guidelines. Most guidelines stipulate that although recent oral intake is not a contraindication to EDPS, it should be one of the factors in deciding how deeply the patient is sedated.[37,38] There has been no report in the medical literature of aspiration during EDPS.[37] Nevertheless, the planned depth of sedation, NPO status, timing of the procedure, and aspiration risk all remain controversial topics in the unique environment of the ED.

Our data demonstrate that propofol seems to be safe in EDPS, and add to the growing body of literature supporting its use. One may also question if the "sedation complication" of brief hypoxemia is harmful. Commonly, studies have defined hypoxemia as a decrease in oxygen saturation to < 90%.[39,40] We defined a sedation complication as hypoxemia, specifically, oxygen saturation < 90% for 10 s or more. Although we included hypoxemia as a sedation complication, it should be noted that little evidence exists as to the clinical significance of transient decreases in oxygen saturation.[41]

In addition to identifying the complications associated with EDPS with propofol, we sought to identify any factors that make it more likely for a patient to sustain these events and complications. Our results suggest that those patients receiving a narcotic with sedation were significantly more likely to develop sedation events or complications than those who did not receive sedation narcotics. Whereas most of the patients received pre-sedation narcotic pain treatment, those who were not treated with sedation analgesia (given < 5 min before the first dose of propofol) were less likely to develop sedation events and complications. This could be of significant importance in the practice of EDPS with propofol and is worth further consideration. We also found that ASA class of systemic disease of the patient correlated significantly with the likelihood of developing a sedation event or complication. Miner et al. reported a respiratory depression rate of 61% in those patients in Class III or higher as compared to our results of 57% of patients with Class III systemic disease sustaining a sedation event or complication of some type.[11] Although we didn't include patients of any classes > III, our results are similar to those of Miner, and there is a significant association of increased ASA systemic disease class and sedation events and complications. Each of these events and complications responded to minimal intervention as they did in patients of all classes.

In conclusion, our results suggest that emergency department procedural sedation with propofol is safe in our population. Brief hypoxemia was the only sedation complication encountered and all episodes readily responded to simple airway maneuvers or increased oxygen concentration. There were no other complications in our study population and no patient required advanced airway maneuvers such as intubation or even positive pressure ventilation. It seems that narcotics given within 5 min of the first dose of propofol increase the likelihood of developing sedation events and complications.

The interpretation of this study is subject to several limitations. The study population was a convenience sample. Also, the overall size of the study was relatively small and under-powered to detect possible statistically significant differences in many of the parameters. The administration of narcotic analgesics was not controlled nor randomized in the study. Therefore, any observed possible associations between narcotic use and hypoxia events should not be interpreted as proving a cause-effect relationship. In addition, the behavior of the emergency staff may have been altered because they were aware they were being observed. Patients were observed in the study only until they appeared to be recovered from sedation. No follow-up data were obtained.


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