Objective: To compile and synthesize the available literature describing medical cannabis use across various disease states. Data Sources: PubMed, EBSCO, and Google Scholar searches were conducted using MeSH and/or keywords. Study Selection and Data Extraction: Studies were included if they described the use of cannabis-based products and medications in the treatment of a predefined list of disease states in humans and were published in English. The extraction period had no historical limit and spanned through April 2019. Data Synthesis: Evidence was compiled and summarized for the following medical conditions: Alzheimer disease, amyotrophic lateral sclerosis, autism, cancer and cancer-associated adverse effects, seizure disorders, human immunodeficiency virus, inflammatory bowel disease, multiple sclerosis (MS), nausea, pain, posttraumatic stress disorder, and hospice care. Relevance to Patient Care and Clinical Practice: Based on identified data, the most robust evidence suggests that medical cannabis may be effective in the treatment of chemotherapy-induced nausea and vomiting, seizure disorders, MS-related spasticity, and pain (excluding diabetic neuropathy). Overall, the evidence is inconsistent and generally limited by poor quality. The large variation in cannabis-based products evaluated in studies limits the ability to make direct comparisons. Regardless of the product, a gradual dose titration was utilized in most studies. Cannabis-based therapies were typically well tolerated, with the most common adverse effects being dizziness, somnolence, dry mouth, nausea, and euphoria. Conclusions: As more states authorize medical cannabis use, there is an increasing need for high-quality clinical evidence describing its efficacy and safety. This review is intended to serve as a reference for clinicians, so that the risks and realistic benefits of medical cannabis are better understood.

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Low vitamin D (serum or plasma 25‐hydroxyvitamin D (25(OH)D)) is a global pandemic and associates with a greater prevalence in all‐cause and cardiovascular mortality and morbidity. Open‐heart surgery is a form of acute stress that decreases circulating 25(OH)D concentrations and exacerbates the preponderance of low vitamin D in a patient population already characterized by low levels. Although supplemental vitamin D increases 25(OH)D, it is unknown if supplemental vitamin D can overcome the decreases in circulating 25(OH)D induced by open‐heart surgery. We sought to identify if supplemental vitamin D protects against the acute decrease in plasma 25(OH)D propagated by open‐heart surgery during perioperative care. Participants undergoing open‐heart surgery were randomly assigned (double‐blind) to one of two groups: (a) vitamin D (n = 75; cholecalciferol, 50,000 IU/dose) or (b) placebo (n = 75). Participants received supplements on three separate occasions: orally the evening before surgery and either orally or per nasogastric tube on postoperative days 1 and 2. Plasma 25(OH)D concentrations were measured at baseline (the day before surgery and before the first supplement bolus), after surgery on postoperative days 1, 2, 3, and 4, at hospital discharge (5–8 days after surgery), and at an elective outpatient follow‐up visit at 6 months. Supplemental vitamin D abolished the acute decrease in 25(OH)D induced by open‐heart surgery during postoperative care. Moreover, plasma 25(OH)D gradually increased from baseline to day 3 and remained significantly increased thereafter but plateaued to discharge with supplemental vitamin D. We conclude that perioperative vitamin D supplementation protects against the immediate decrease in plasma 25(OH)D induced by open‐heart surgery. ClinicalTrials.gov Identifier: NCT02460211.

The use of prophylactic anticonvulsants to prevent early post-traumatic seizures (PTSs) is recommended but inconsistently employed in patients with traumatic brain injury (TBI). The authors evaluated outcomes associated with prophylaxis administration in patients with TBI at a Level 1 trauma center. All patients admitted with TBI from October 2007 through May 2012 were included. Our primary outcome was the incidence of early PTSs. Secondary outcomes included mortality, length of hospital and intensive care unit (ICU) stays, and incidence of late seizures. Of the 2,111 patients with TBI, 557 (26.4%) received seizure prophylaxis and 1,554 (73.6%) did not. Two early PTSs occurred in the prophylaxis group (0.4%), whereas 21 occurred in the non-prophylaxis group (1.4%) (p = 0.05). The overall mortality rate was higher in patients who received prophylaxis (14.2% vs. 6.2%; p < 0.001), and the mean hospital length of stay (LOS) was longer (6.8 ± 6.9 vs. 3.8 ± 5 days; p < 0.001). In patients with severe and moderate TBI, the rate of prophylaxis administration was approximately half, whereas significantly fewer patients with mild TBI received prophylaxis than did not (20.2% vs 79.8%, p < 0.001). Lower Glasgow Coma Scale (GCS) score and longer hospital LOS were associated with early PTS (p = 0.008 for both comparisons), but sex and age were not. Brain hemorrhage was present in 78.3% of those patients who experienced early seizures. In our cohort, patients who received seizure prophylaxis had a lower GCS score, higher overall mortality rate, longer LOS, and more frequent ICU admissions, suggesting that patients who received prophylaxis were likely more severely injured.