This morning my patient was a 62 year old female who uses marijuana daily. She also reported to me that after a recent general anesthetic she experienced a two week period of amnesia immediately following her anesthetic. She stated that she performed all of her normal activities and that friend and family told her she behaved normally, however, she states that she has no recall of the events during these two weeks.
My anesthetic was a straight general endotracheal anesthetic using a propofol infusion for its benefits on PONV, and inhalation anesthesia to facilitate neuromuscular blockade during surgery as well as reduce the required propofol infusion dose. I gave hydromorphone 2 mg up front with 2 mg of versed. I also gave 4 mg of decadron as we rolled to the OR. I placed a BIS monitor to evaluate her EEG in real time as well as her BIS. I was particularly motivated to avoid burst suppression given her recent history of memory loss after anesthesia. I suspected that perhaps the patient had developed some mild post operative delirium (POD), and increasing frequency of burst suppression during anesthesia is associated with increased rates of POD.
On induction, I gave the patient 110 mg of propofol. I noted that the BIS quickly went to about 20 and the burst suppression ration (BSR) increased to nearly 40%. I was also able to note a flat EEG indicating burst suppression. This indicated immediately to me that the patient likely had a vulnerable brain. Therefore, I immediately planned for a lower setting on the sevoflurance concentration and propofol infusion. I titrated the sevoflurane to an ET% of 0.9 (MAC 0.4) and propofol of 75 mcg/kg/min. However, with more time, her BIS recovered but then drifted lower. I titrated the propofol infusion down to a minimum of 30 mcg/kg/min with the SEVO at 0.5 MAC (age adjusted). At this level the BIS hovered near 40 with BSR remaining at 0. Due to the very low anesthetic dose I was providing I opted to give 5 mg vecuronium with small intermittent doses to reduce the chance of sudden movement. In fact, prior to incision and no stimulus to the patient and the BIS reading 39, the patient began coughing spontaneously. This highlights the fact that a BIS of 40 will NOT prevent patient movement during surgery. This event prompted me to decide to maintain some degree of paralysis. In my previous post on POD, I cited a study showing that the incidence of POD was decreased when the BIS was titrated to 50 vs. a BIS of 35. I would emphasize that the patient's heart rate and blood pressure all remained suppressed but WNL during induction and the entirety of the case and did not seem to be entirely associated with her BIS level.
This patient was a daily marijuana user. Marijuana is smoked for its THC content, which is an agonist at both the endocanabinoid 1 and 2 receptors. The CB1 receptor is found in the CNS. CB 1 receptors seem to primarily modulate pain, memory, and energy metabolism. CB 2 receptors are located in both the CNS and immune cells and modulate the immune signaling as well as the inflammatory response. CBD also has actions on the 5-HT1a receptor (serotonin) in the CNS and platelets resulting in its anti nausea effects.
Acute Marijuana use (canabinoid intoxication) results in a number of effects. These include tachycardia and vasodilation. In patients with CAD, this has resulted in increased incidence of angina and even MI (via demand ischemia). Typically these affects resolve after 1 hour from canibinoid use. Nevertheless, in a large retrospective review of over 27,000 records, the active cannabinoid users had increased odds of experiencing a myocardial infarction in the preoperative period. Bronchodilation with hyperreactivity of the airways is also associated with acute cannabis use. In the CNS, cannabis use causes anxiolysis or anxiety, paranoia or even frank psychosis, euphoria, dizziness, headache, memory dysfunction and analgesia. Furthermore, in young users the risk of stroke compared to tobacco smokers was 4.7 times higher. This effect may be a result of the vasoconstriction effect on cerebral vessels of cannabis when hypoxia or hypercapnia is present. Furthermore, prolonged heavy use of cannabinoids results in hippocampal thinning and neuronal death. Acute cannabis use can also be an antiemetic as well as increasing appetite. Chronic daily users may see increased atheromatous disease, COPD or emphysema, and some may experience increased nausea and vomiting (hyperemesis). In patients experience hyperemesis, severe abdominal pain is often an accompanying symptom.
Typically chronic marijuana users presenting for surgery are stopping their use prior to arrival. This presents the anesthesiologist with the possibility of withdrawal symptoms. Withdrawal symptoms include irritability, anger, aggression, anxiety, nervousness, insomnia, disturbed dreams, restlessness, depressed mood, anorexia, abdominal cramping, tremors, sweating, fevers, chills and headache. This withdrawal syndrome can last for several weeks in high dose chronic users.
Cannabis use and its effects on anesthetic requirements in humans have not been well studied. In one study on admitted cannabis users demonstrated that they required significantly higher propofol doses than non users to achieve a BIS of < 60. In another study, patients given a synthetic THC during a general anesthetic resulted in an increase in the BIS. From this study, it was not clear whether the increase in BIS represented a lightening of anesthesia, or the effects of the cannabis on the processed EEG. Despite these studies, in my patient, it was clear that a small propofol dose had a profound effect on her BIS. Perhaps this is reflective of the effects of prolonged chronic cannabis use on the brain. Unfortunately, we have no well done studies to establish this. Nevertheless, I believe that given her reaction, it is at least prudent to be alerted to this possibility in older chronic daily marijuana users. This may be a relative indication to place a pre induction BIS monitor on for better titration of induction agents.
Recently, during another case where I was working with a CRNA, we had a patient who used marijuana with some frequency. The CRNA stated that the patient was at risk from aspiration and should be treated as if they were a "full stomach"; i.e. RSI with endotracheal intubation to prevent aspiration. In a recent search of the literature, I was able to find a case report where a patient who was a heavy chronic marijuana user having an elective surgery with LMA, vomited during surgery and required emergent RSI intubation during the surgery. The providers placed an OG tube and suctioned out 600cc's of gastric content. In this article, the blame for the patient have gastric contents was placed on his use of marijuana. In some cases, marijuana is associated with a hyperemesis syndrome. However, it is not clear that this is due to delayed gastric emptying, but rather results from cannabis effects on the vomiting center of the brain. In 2023, an RCT was published where cannabidiol was used to treat patients with gastroparesis. The authors were able to show in these patients that symptoms improved with cannabidiol. Whether cannabinoids can decrease gastric emptying, it seems unclear. Therefore, in patients with heavy cannabis use, it seems prudent to question them to determine if they have trouble with early satiety, nausea, vomiting or repeated belching and reflux. If they are free of any of these symptoms, there is no evidence that heavy chronic cannabis users need to treated as if they have a full stomach.
With regards to intraoperative analgesia, again there are no well done studies to guide us. However, recent studies do indicate that cannabis users report higher pain scores, have worse sleep, and require more rescue analgesics in the immediate post operative period. Studies on cannabinoid agonists have shown that they facilitate endogenous opioid signaling and increase concentrations of endogenous opioids. In animal studies cannabinoids and opioids are synergistic
Ketamine induces endogenous cannabinoid release which may partially explain its role in an anti-nociception. However, the psychomotor side effects of ketamine are enhanced with CBD administration. It also appears that gabapentin and cannabinoids act synergistically both acting in similar manner as activation of CB receptors results in inhibition of the voltage dependent calcium channel similar to gabapentin. Thus care should be taken when gabapentinoids are part of an ERAS protocol and the patient is a heavy cannabis user.
In summary, patient coming to surgery who are chronic heavy users of marijuana seem to be at increased risk of perioperative strok and MACE. Fortunately, the 1/2 life of THC is rather short, and therefore, it is unlikely that patients presenting for elective surgery will be directly affected by high levels of cannabinoids. However, it is well documented that acute cannabis intoxication will likely result in tachycardia with vasodilation, placing these patients at potential risk for hemodynamic instability. At this time it is unclear if chronic heavy users of cannabis have higher anesthetic requirements, although some studies suggest this. In this case report, the patient have very low anesthesia requirements, and in fact, processed EEG monitoring suggested the patient had a vulnerable brain, driving me to significantly titrate down the anesthetic level to avoid post operative delirium.
1. Zheng T, BouSaba J, Taylor A, Dilmaghani S, Busciglio I, Carlson P, Torres M, Ryks M, Burton D, Harmsen WS, Camilleri M. A Randomized, Controlled Trial of Efficacy and Safety of Cannabidiol in Idiopathic and Diabetic Gastroparesis. Clin Gastroenterol Hepatol. 2023 Dec;21(13):3405-3414.
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