ABSTRACT
Excessive alcohol consumption and alcohol use disorder (AUD) increase the risk of perioperative morbidity and mortality. Aspiration, malnutrition, coagulopathies, seizures, and hemodynamic alterations are only a few of the major concerns related to acute alcohol intoxication and AUD. There are also numerous physiological effects, changes in medication metabolism and pharmacology, and adverse events related to chronic alcohol consumption. These are all important considerations for the anesthesiologist in the perioperative management of a patient with AUD. Pain perception and thresholds are altered in patients with acute and chronic alcohol use. Medications used to manage AUD symptoms, particularly naltrexone, can have significant perioperative implications. Patients on naltrexone who continue or stop this medication in the perioperative period are at an increased risk for undertreated pain or substance use relapse. This review highlights key considerations for the anesthesiologist and pain physician in the perioperative management of patients with active AUD (or those in recovery). It discusses the effects of acute and chronic alcohol use on pain perception and thresholds, provides guidance on the perioperative management of naltrexone and low-dose naltrexone, and reviews a multimodal approach to pain management.
ABSTRACT
Urticaria within one hour of lidocaine injection is a sign of type I (immediate) hypersensitivity to lidocaine, yet most patients suspected of having a lidocaine allergy do not exhibit urticaria. Aside from being a sign of a rare lidocaine allergy, urticaria can also be a symptom of COVID-19. COVID-19 patients who experience urticaria after receiving lidocaine require careful evaluation to determine the cause. Here, we present a case of a patient exhibiting urticaria one hour after a lidocaine injection for the Pecto-intercostal nerve block to treat COVID-19-induced costochondritis.
ABSTRACT
INTRODUCTION: Celiac plexus neurolysis (CPN) has been verified for mitigating pancreatic cancer pain. However, information regarding CPN's use beyond this remains limited. OBJECTIVES: Identify which cancers benefit from CPN, which symptoms improve, and when symptoms improve. METHODS: Retrospective analysis was conducted on 173 patients who received CPN for pain caused by various malignancies. Mean symptom changes on the MD Anderson Symptom Inventory (MDASI) from baseline to 2 weeks, 1 month, and 2 months after CPN were analyzed overall and then by cancer type: pancreatic (all stages and stages III-IV), hepatobiliary, and nonpancreatic, nonhepatobiliary gastrointestinal (NPNH-gastrointestinal). RESULTS: Eighty-two pancreatic, 43 NPNH-gastrointestinal, 14 hepatobiliary, and 34 patients with other cancers met inclusion criteria. Statistically significant changes included decrease in the pain score at 1 month by 1.01 points for all cancers, 1.65 points for all pancreatic cancers, and 1.88 points for late-stage pancreatic cancers. At 2 months, pain decreased by 1.50 points for all cancers, 1.68 points for all pancreatic cancers, 2.37 points for late-stage pancreatic cancers, and 1.50 points in NPNH-gastrointestinal cancers. At 2 months, quality of life improved by 1.07 points for all cancers and 1.53 points for all pancreatic cancers. Sleep improved at 2 months for all cancers by 0.73 points and 1.60 points in late-stage pancreatic cancers. At 2 months, pancreatic cancer patients improved in general activity by 0.93 points, walking by 1.00 points, and working by 1.12 points. CONCLUSION: Celiac plexus neurolysis can decrease cancer symptom burden beyond pain including quality of life and sleep for pancreatic and nonpancreatic cancers, as well as general activity for pancreatic cancers.
ABSTRACT
Angiotensin II (Ang II) modulates blood pressure and atherosclerosis development through its vascular type-1 (AT1R) and type-2 (AT2R) receptors, which have opposing effects. AT2R activation produces hypotension, and is anti-atherogenic. Targeted overexpression of AT2Rs in vascular smooth muscle cells (VSMCs) indicates that these effects are due to increased nitric oxide (NO) generation. However, the role of endogenous VSMC AT2Rs in these events is unknown. Effect of 7-day low-dose Ang II-infusion (12 µg/kg/hr) on blood pressure was tested in 9-week-old apoE((-/-)) mice fed a low or high cholesterol diet (LCD or HCD, respectively). Cardiac output was measured by echocardiography. Immunohistochemistry was performed to localize and quantify AT2Rs and p-Ser(1177)-endothelial nitric oxide synthase (eNOS) levels in the aortic arch. PD123319 and GW-9662 were used to selectively block the AT2R and peroxisome proliferator-activated receptor-γ (PPAR-γ), respectively. Ang II infusion decreased blood pressure by 12 mmHg (P < 0.001) in LCD/apoE((-/-)) mice without altering cardiac output; a response blocked by PD123319. Although, AT2R stimulation neither activated eNOS (p-Ser(1177)-eNOS) nor changed plasma NO metabolites, it caused an ~6-fold increase in VSMC PPAR-γ levels (P < 0.001) and the AT2R-mediated hypotension was abolished by GW-9662. AT2R-mediated hypotension was also inhibited by HCD, which selectively decreased VSMC AT2R expression by ~6-fold (P < 0.01). These findings suggest a novel pathway for the Ang II/AT2R-mediated hypotensive response that involves PPAR-γ, and is down regulated by a HCD.
