Bryson also concluded based on his review of the literature, that the pulmonary complications in the chronic marijuana smoker are equivalent to those seen in the chronic tobacco smoker, while Wu et al. estimated that 3e4 cannabis cigarettes daily equates to about 20 tobacco cigarettes in terms of bronchial tissue damage. Cannabis use has also been linked to a higher risk in cancers, possibly due to the increased carcinogens entering the airway. Similar to tobacco use, marijuana use plays a significant role in the development of lung cancer. In a case control study performed in New Zealand, young adults had an 8% increase in lung cancer risk for each joint year of cannabis smoking after adjusting for the cofounders, such as age, sex, ethnicity and family history. Berthiller et al. pooled data from a multitude of institutions across multiple countries, comprising of over 1200 patients, and reported an increased risk of lung cancer for every marijuana use. In addition, a 40 year cohort study with about 48,000 patients reported an increased risk of lung cancer in young men who had smoked marijuana more than 50 times. This study was limited however by the nature of patient self-reporting. Head and neck cancers have also been theorized to be at a higher risk similar to that of tobacco smoking. However, a pooled analysis performed by Berthiller et al. found that infrequent marijuana smoking did not confer a greater risk after adjusting for cofounders. The authors did note that due to the low prevalence of frequent smoking within the study population, that a moderately increased risk could not be ruled out. In another population based case control study, there was an increased incidence of head and neck cancers in patients with a 30 joint-year history, yet the association did not exist when accounting for tobacco smoking suggesting the risk is greater with tobacco than marijuana grow system.
In a crosssectional study conducted by Mills et al., the rate of marijuana use via patient self-reporting was found to be 14% amongst surgical patients in 2003. This led the authors to conclude that questions about illicit drug use should be a routine part of the preanesthetic assessment, especially in patients that the anesthesiologist finds hard to settle, due to anxiety or other psychologic manifestations, because of the potential anesthetic complications that may occur. In a series of case reports, Guarisco presented three patients who suffered from significant respiratory distress due to isolated uvulitis, a disease of low incidence typically associated with infection or traumatic irritation from instruments used in the airway. Investigating further, all three patients were found to have inhaled large quantities of cannabis within six to twelve hours of the onset of symptoms leading to the conclusion of a possible correlation with inhaled irritants such as cannabis. Due to known cases of isolated uvulitis and the possible link with marijuana, the authors suggest that toxicology urine and blood studies for THC should be performed in cases where marijuana use is suspected but not confirmed by history taking. Multiple other cases have also been reported with similar findings. In a case series by Sloan, three adolescents suffered acute uvular inflammation post the heavy use of marijuana, having smoking at least three marijuana cigarettes, despite negative throat cultures. In 1971, a cohort study was performed in which a large quantity of marijuana, over 100 grams, was smoked over several months. Of the 31 subjects, almost half suffered from recurrent rhinopharyngitis as well as developed acute uvular edema after the heavy marijuana inhalation which lasted approximately 12e24 hours. These findings stress the importance in the maintenance of the airway during anesthesia following acute marijuana use due to the potential airway obstruction that may occur. In fact, in presenting a case of uvular edema and airway obstruction with cannabis inhalation 4 hours prior to surgery, Pertwee recommended that elective operations should be avoided altogether if a patient was recently exposed to cannabis smoke. This recommendation seems reasonable when taking into consideration the life-threatening bronchospasm leading to asphyxia, brain damage or death resulting from tracheal intubation in patients with obstructive airways.
One proposed course of action has been the therapeutic use of steroids. In Guarisco’s study, he theorized that steroids should help inhaled irritant uvulitis.As steroids increase endotracheal permeability, decrease mucosal edema and stabilize lysosomal membranes, thus decreasing the inflammatory response, the theory has scientific basis. In a prospective, randomized, double-blind study, Silvanus et al. found that the addition of methylprednisolone to salbutamol in patients with a partially reversible airway obstruction helped in the diminution of the reflex bronchoconstriction that can result from tracheal intubation. This led to Hawkins et al.’s recommendation that at the first signs of airway obstruction, dexamethasone should be used as the drug of choice, 1 mg/kg every 6e12 hours over the course of one to two days.This recommendation gained credence in the dramatic relief that dexamethasone provided in the post-traumatic cases. However, Mallat et al. concluded that although marijuana-induced uvular edema is a serious postoperative complication that has a potential for simple treatment, in the case of an elective surgical procedure with an acute history of cannabis exposure, surgery should be cancelled as prophylactic treatment may not be efficient.The complications of the airway are not limited to intubation however. The inhalation of toxic chemicals as well as smoke can cause laryngospasm by chemoreceptor stimulation. In addition, the inhalation of hot gasses can trigger laryngospasm via thermoreceptor stimulation, especially in the case of lowered sensory afferent neuron threshold potentials such as in light anesthesia. In line with this, White presented a case in which a known cannabis smoker suffered severe laryngospasm following extubation.As found within the reviews, multiple observations have been made showing crosstolerance between marijuana and barbiturates, opioids, prostaglandins, chlorpromazine and alcohol. In addition, animal studies have shown additive effects amongst them all except for alcohol. These drug interactions have led to further exploration of its reactions to other medication groups. As a result of fat sequestration and subsequent slow elimination from the tissues,cannabinoids may be present to interact with multiple anesthetic agents.
In Symons’s case report, the patient required multiple boluses of propofol and two additional doses of midazolam to achieve appropriate sedation.In a prospective, randomized, single-blind study of 60 patients, chronic marijuana users required significantly increased doses of propofol to facilitate successful insertion of the laryngeal mask and thus suggesting that the increased doses, in chronic marijuana users, may be a requirement for appropriate loss of consciousness as well as jaw relaxation and airway reflex depression. The authors theorized that the variations in the level of delta9-THC can explain variations in propofol responses. In a review written in the American Association of Nurse Anesthetists Journal, Dickerson reported the synergistic effects of cannabis to include: potentiation of nondepolarizing muscle relaxants, potentiation of norepinephrine, the augmentation of any drug causing respiratory or cardiac depression, as well as a more profound response to inhaled anesthetics sensitization of the myocardium to catecholamines due to the increased level of epinephrine. On the subject of muscle relaxants, THC depletes acetylcholine stores and exerts an anticholinergic effect and thus creates a potentiation of the nondepolarizing muscle relaxants. A review by Hall et al. explored THC’s interaction with drugs affecting heart rate and arterial pressure and found that due to cannabis’s own cardiovascular effects,it may interact with medications such as beta-blockers, anticholinergics and cholinesterase inhibitors.Due to these potential autonomic reactions, as well as theoretical psychiatric complications, such as withdrawal effects and their interference with anesthetic induction or postoperative recovery, there has been a stress made to inquiring about drug history or avoiding elective operations altogether. Dickerson, in his review, recommended that, due to all potential effects and interactions, not only should an extensive history of drug use be elicited at the time of the preoperative assessment, including the frequency of use and time of last use, but that anesthesia should be avoided in any patient with cannabis use within the past 72 hours. This gained further credibility in a randomized, double-blind trial, in which an apparent drug interaction was observed in the patient population who underwent general anesthesia within 72 hours of marijuana use leading to a sustained postoperative tachycardia, a finding potentially due to an interaction between cannabinol metabolites and atropine administration during anesthesia.
One of the most researched and known risk factor for perior postoperative complications, increased hospitals costs and resource usage is smoking, specifically tobacco smoke. In fact, the rates of perioperative respiratory events, such as reintubation, hypoventilation, hypoxemia, laryngospasm, bronchospasm, and aspiration, have a total incidence of 5.5% in smokers compared to 3.1% in nonsmokers, making these events 70% more prevalent with smoking. In addition, in a randomized controlled trial out of Denmark, orthopedic surgery patients who smoked were compared to those who underwent cessation counseling and nicotine replacement therapy. In the study, they found an overall complication rate of 18% compared to the 52% found in the smoking group, including a cardiac event rate of 0% compared to 10%. A similarly designed study found a significant relative risk reduction of 49% for not only systemic complications but that of wounds as well. These call into question the role of marijuana on perioperative complications, especially when taking into consideration that the pulmonary complications in the chronic cannabis smoker are equivalents to that of a chronic tobacco smoker, probably due to the cannabis vertical farming smoke products.One such pulmonary complication is airway obstruction, extensively linked to marijuana use, in which Warner et al. found that untreated, such as a lack of smoking cessation in the case of marijuana, leaves patients at a high risk for perioperative complications.When it comes to the case of cardiovascular maintenance in the perioperative period, marijuana presents complications. As mentioned previously, cannabis use can create a series of ECG changes that must be considered and monitored such as PVCs, atrial fibrillation, AV block,or Brugada-like changes. As a worst case scenario, cannabis use has been linked to plaque rupture and resultant myocardial infarction. These are all causes for concern considering that Gregg et al. reported, in conducting a series of 55 clinical trials in patients medicated with THC, that peak heart rate increased by 24.1% in surgical patients compared to the non-surgical. The authors concluded that THC may have a synergistic cardiovascular relationship with surgical stress. This tachycardia gave credence to Bryson’s recommendation that ketamine, pancuronium, atropine and epinephrine, all drugs known to affect heart rate, should be avoided in patients with history of acute marijuana use, while the bradycardia and hypotension that results from high doses of marijuana called into question the amount of atropine and vasopressors needed. Despite the impetus behind these recommendations, 1 trial showed epinephrine to have no synergistic effect with marijuana when it comes to cardiovascular effects, showing more research is needed on the potential interactions of marijuana and perioperative medications.
Field visualization plays a key role in any operation. Marijuana, however, may affect this. In a literature review published in Poland, Zakrzeska et al. explored how cannabinoids and their metabolites and their effects on the receptors CB1, CB2, CBPT and CBED as well as other systems may impact hemostasis.The authors concluded that despite the studies that have shown contradictory effects, based on the physiology, it is reasonable to conclude that marijuana could have an anti-hemostatic effect. Multiple studies have backed up that conclusion. In 1979, Schaeffer et al. reported that cannabis users had a diminished ability for platelet aggregation.This led to further investigations and in 1989, Formukong et al. looked at cannabinoids’ effect on platelet aggregation. The authors found that in both rabbit and human platelet aggregation that was induced by adenosine diphosphate or epinephrine was inhibited by cannabinoids in a dose-dependent manner and with cannabidiol more potent than THC in this effect. Then in 2007, an in vitro coagulation study showed that marijuana and two of the major cannabinoids, including THC, had an anticoagulant property and even more so, an antithrombotic effect. In the in vivo model testing clotting times of lean and obese rats, those treated with cannabis had clotting times 1.5 to 2 times greater than the controls, thus supporting the results of the in vitro study.