Recently at our hospital a 25 year old female presented with acute cholecystitis for lap cholecystectomy. She was healthy, but expressed a large degree of anxiety regarding the procedure and anesthesia. When it was time to roll back to the OR, her premedication was administered (a 5 cc syringe of 2cc versed (2mg), 2cc fentanyl (100mcg) and 1 cc decadron (4mg)).
The patient appeared to lose consciousness in the appropriate amount of time and as she entered the OR was apneic. She was administered oxygen and mask ventilated. Saturations and blood pressure were 98% and 160's systolic. I was called into the room for consultation when it was realized that the 5 cc syringe of rocuronium had been mistakenly given to the patient in preop and that the 5 cc syringe of the versed/fentanyl cocktail had not been. This cocktail was immediately administered and anesthesia induced. I noted that the patient was apparently unconscious, but very sweaty with elevated blood pressure.
After induction and intubation, the case proceeded uneventfully. 0/4 twitches were observed at this point on the twitch monitor confirming that the patient had received a muscle relaxant. The question posed to me by the CRNA was is it possible to induce retrograde amnesia so that the one to two minutes prior to induction when the patient was apparently completely paralyzed would be lost to memory. My first response was that I didn't believe there was any foolproof method known to induce retrograde amnesia.
In anesthesia, we often give midazolam to induce anterograde amnesia. Studies have been conducted looking for retrograde amnesia with midazolam, but have been unable to demonstrate this characteristic [1-3]. However, there is a case report of severe and long term retrograde amnesia after anesthesia that was reversed within one minute of giving flumazenil to reverse versed that had been given prior to surgery.
In the case at hand, there was no expectation that we could induce retrograde amnesia of being paralyzed by the patient. However, a plan was executed that involved giving an extra dose of versed (2mg) immediately. Sevoflurane was used and dialed up to 3% End tidal as long as blood pressure tolerated this. Towards the end of the case, an additional 200 mg of propofol was titrated in as the sevoflurane was dialed down. Also, during the case, an additional 100 mcg of fentanyl was used on top of the fentanyl that would have been considered adequate. In this case that came to a total of 300 mcg of fentanyl. As the case finished, the propofol was titrated in as long as blood pressure and heart rate were adequate to 200mg and the sevoflurane discontinued. The patient was taken to PACU breathing spontaneously, but intubated and unresponsive. After about 10 min in PACU, she was extubated uneventfully and after another 30 min was evaluated for recall. She remained about 90 min total in PACU. At no time during her PACU stay did she indicate that she had any recall of having been unable to move prior to surgery.
So, in essence, an attempt to induce a mild form of POCD in the hopes of preventing recall was attempted. POCD is a hot topic in the current literature. Although, it is clear that those at risk are older patients with significant comorbid disease and preoperative cognitive decline, it seems to be that POCD doesn't seem to be caused (at least long term) by anesthetics. Important to our discussion, is POCD increased by increasing depth of anesthesia. Several papers have been published trying to determine a causal link between deeper anesthesia and POCD. Out of six papers looking at this, three found no difference, and two found that deeper anesthesia was actually protective, while a one did find an association between deeper anesthesia and POCD. However, in terms of post operative delirium, deeper anesthesia is definitively associated with higher rates of delirium. However, this is a transient phenomenon, and is not relevant to our current concern, that of decreasing the ability to retrieve or recall events immediately prior to surgery due to an episode of inadvertent chemical paralysis.
This may be a case report of retrograde amnesia, from slightly deeper than typical general anesthesia. However, it is very difficult to make this determination definitively as, the patient may have developed recall of these events after discharge. In addition, there is the potential for implicit recall, which is different from explicit recall. Implicit recall is when the brain does retain "memory" of events, but in the subconscious realm. This can lead to unexplained PTSD like symptoms in some patients who have no conscious memory of the traumatic event during surgery.
There is no reason to believe that rocuronium induced amnesia or plays a role in amnesia or sedation. However, as NDMB do block acetyl choline receptors, and these are prominent in the brain, this possibility does have some merit.
1. Hupp JR, Becker LE. Intensity and duration of amnesia from intravenous midazolam given for sedation. Conn St Dent Assoc J 1988;62:80-5.
2. Oboyle CA. Benzodiazepine-induced amnesia and anaesthetic practice: a review. Psychopharmacol Ser 1988;6:146-65.
3. Twersky RS, Hartung J, Berger BJ, et al. Midazolam enhances anterograde but not retrograde amnesia in pediatric patients. Anesthesiology 1993;78:51-5.
4. Koht A, Moss JI. Does Midazolam Cause Retrogramde Amnesia and can flumazenil reverese that Amnesia? A&A 1997;85(1). 211-12.