Marijuana has also been reported as a risk factor for stroke. Over 80 cases have been reported in which patients had strokes, with a higher prevalence of ischemic strokes, that were associated with either a recent increase, in the days leading up to the event, or chronic history of heavy marijuana use. They believed that the marked swings in blood pressure or the reversible cerebral vasoconstriction that resulted from marijuana use were likely mechanisms of stroke but admitted that no firm conclusions could be drawn without further studies.In addition, Lawson reported a similar belief that drug induced vasospasm was a plausible explanation for TIAs, but also with the caveat that due to the confounding medications/illicit substances being used in his patient, no direct association could be determined. Also of interest is marijuana use’s effect on other cardiovascular vessels. When cohort studies were performed comparing marijuana users with resultant limb arteritis to patients suffering from thromboangiitis obliterans, marijuana associated arteritis occurred in younger, usually male patients with a unilateral, lower limb as the common presentation.Due to the unfiltered nature of the marijuana cigarette compared to commercially available tobacco cigarettes,grow table the amount of carcinogens and irritants, like tar, that enter the upper airway is increased with approximately a three-fold increase in tar inhalation and one third more tar deposition in the respiratory tract.

More specifically, the tar produced from cannabis smoke contains greater concentration of benzanthracenes and benzopyrenes than tobacco smoke. In addition, as compared to smoking tobacco, there is a two-thirds greater puff volume, one-third greater depth of inhalation and a four-fold longer breath-holding time, all of which are common practices to try to maximize THC absorption, which is around 50% of cigarette content. These practices result in five times the amount of carboxyhemoglobin levels as compared to the typical tobacco smoker despite the presence of similar quantities of carbon monoxide from the incomplete combustion of the organic compounds found within each product. In reporting his case, Schwartz theorized that high temperatures in which marijuana burns compared to tobacco may increase the irritancy of marijuana to the mucous membranes. While the higher temperature is a possibility, the evidence of marijuana’s irritancy is well documented. In a cohort study comprised of 40 healthy patients, Roth et al. showed that cannabis smokers had significantly increased visual bronchitis index scores resulting from large airway epithelial damage, edema, and erythema. On mucosal biopsy, goblet cell hyperplasia with subsequent increase in secretions, loss of ciliated epithelium and squamous metaplasia were also present in 97% of smokers. They concluded that marijuana use is associated with airway inflammation that is similar to that of a tobacco smoker. A cross-sectional study on over 6000 patients, from 1988 to 1994, found an increased incidence of chronic bronchitis symptoms such as wheezing and productive cough occurring in patients 10 years younger, on average, than tobacco smokers. Case-control trials performed found similar findings with regards to increases in wheezing, shortness of breath, cough and phlegm as well as the similarities with tobacco use. 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 casecontrol 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.Marijuana’s prevalence is evident amongst all patient populations. In a cross sectional 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 lysosomalmembranes, thus decreasing the inflammatory response, the theory has scientific basis. In a prospective, randomized,4×8 grow table with wheels 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 can celled as prophylactic treatment may not be effiffifficient. 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 cross tolerance 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. Areview 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%.