Anesthetic Management Guided by Transthoracic Echocardiography During Cesarean Delivery Complicated by Hypertrophic Cardiomyopathy.

We describe the management of a parturient woman with hypertrophic cardiomyopathy who developed a symptomatic accelerated idioventricular rhythm who required an urgent cesarean delivery at 32 weeks. Transthoracic echocardiography helped guide anesthetic management, including epidural dosing, fluid management, and phenylephrine infusion rates. This case demonstrates the application of transthoracic echocardiography to guide anesthetic management in a parturient woman at risk for cardiovascular compromise.

Physostigmine reverses disturbances of the intestinal microcirculation during experimental endotoxemia.

Intestinal microcirculatory disturbances play an important role in the pathophysiology of sepsis. A neural anti-inflammatory pathway has been suggested as a potential target for therapy that may dampen systemic inflammation. The aim of this study is to investigate the effects of physostigmine, a cholinesterase inhibitor, on the intestinal microcirculation and vascular contractility in experimental endotoxemia. Endotoxemia was induced in Lewis rats by intravenous lipopolysaccharide (LPS) administration. Animals were treated with either physostigmine or saline (control) following LPS challenge. The intestinal microcirculation, including leukocyte-endothelial interaction, functional capillary density (FCD) and non-perfused capillary density (NCD), was examined by intravital microscopy (IVM) 2 hours after LPS administration. The impact of physostigmine on vascular contractility of rat aortic rings was examined by in vitro myography. Physostigmine significantly reduced the number of adhering leukocytes in intestinal submucosal venules (V1 venules: -61%, V3 venules: -36%) of LPS animals. FCD was significantly increased by physostigmine treatment (circular muscle layer: +180%, longitudinal muscle layer: +162%, mucosa: +149%). Low concentrations of physostigmine produced significant contraction of aortic ring preparations, whereas high concentrations produced relaxation. In conclusion, physostigmine treatment significantly improved the intestinal microcirculation in experimental endotoxemia by reducing leukocyte adhesion and increasing FCD.

Cannabinoid receptor 1 inhibition causes seizures during anesthesia induction in experimental sepsis.

We report on seizures during anesthesia induction in animals treated with a cannabinoid receptor 1 (CB1R) antagonist for experimental sepsis. Animals received surgery for colon ascendens stent peritonitis-induced sepsis or sham surgery followed by treatment of CB1R antagonist, CB1R agonist, or placebo. Fourteen hours later, animals received pentobarbital or ketamine for anesthesia induction and animal behavior was observed. Tonic-clonic seizures were observed in 5 of 12 septic animals (42%) treated with CB1R antagonist after induction of anesthesia with pentobarbital. The data suggest that CB1R inhibition in combination with pentobarbital may increase the incidence of anesthetic-induced seizures in the case of sepsis.

Cannabinoid receptor 2 activation reduces intestinal leukocyte recruitment and systemic inflammatory mediator release in acute experimental sepsis.

INTRODUCTION: Cannabinoid receptor 2 (CB2R) expression is upregulated during sepsis. However, there are conflicting results regarding the effects of CB2R modulation in the hyperinflammatory phase of the disease. The aim of this study was therefore to investigate the effects of CB2R manipulation on leukocyte activation within the intestinal microcirculation in two acute experimental sepsis models. METHODS: In the endotoxemia model we studied four groups of Lewis rats: controls, lipopolysaccharide (LPS), LPS + CB2R agonist HU308 (2.5 mg/kg), and LPS + CB2R antagonist AM630 (2.5 mg/kg). In the colon ascendens stent peritonitis (CASP)-induced sepsis model we also studied four groups: sham group, CASP and CASP + CB2R agonist (HU308, 2.5 or 10 mg/kg). Intravital microscopy was performed 2 hours following LPS/placebo administration or 16 hours following CASP/sham surgery to quantify intestinal leukocyte recruitment. Additionally, hemodynamic monitoring, histological examinations and measurements of inflammatory mediators were performed. RESULTS: HU308 administration significantly reduced intestinal leukocyte adhesion in both acute sepsis models. The systemic levels of inflammatory mediators were significantly reduced by 10 mg/kg HU308 treatment in CASP animals. CONCLUSION: CB2R activation reduces leukocyte activation and systemic release of inflammatory mediators in acute experimental sepsis. Drugs targeting the CB2R pathway may have therapeutic potential in sepsis.

Activated protein C improves pial microcirculation in experimental endotoxemia in rats.

INTRODUCTION: The brain is one of the first organs affected clinically in sepsis. Microcirculatory alterations are suggested to be a critical component in the pathophysiology of sepsis. The aim of this study was to investigate the effects of recombinant human activated protein C (rhAPC) on the pial microcirculation in experimental endotoxemia using intravital microscopy. Our hypothesis is rhAPC protects pial microcirculation in endotoxemia. METHODS: Endotoxemia was generated in Lewis rats with intravenous injection of lipopolysaccharide (LPS, 5 mg/kg i.v.). Dura mater was removed through a cranial window to expose pial vessels on the brain surface. The microcirculation, including leukocyte-endothelial interaction, functional capillary density (FCD) and plasma extravasation of pial vessels was examined by fluorescent intravital microscopy (IVM) 2 h after administration of LPS, LPS and rhAPC or equivalent amount of saline (used as Control group). Plasma cytokine levels of interleukin 1 alpha (IL1-α), tumor necrosis factor-α (TNF-α), interferon γ (IFN-γ), Monocyte chemotactic protein-1 (MCP-1) and Granulocyte-macrophage colony-stimulating factor (GM-CSF) were evaluated after IVM. RESULTS: LPS challenge significantly increased leukocyte adhesion (773±190 vs. 592±152 n/mm(2) Control), decreased FCD (218±54 vs. 418±74 cm/cm(2) Control) and increased proinflammatory cytokine levels (IL-1α: 5032±1502 vs. 8±21 pg/ml; TNF-α: 1823±1007 vs. 168±228 pg/ml; IFN-γ: 785±434 vs. 0 pg/ml; GM-CSF: 54±52 vs. 1±3 pg/ml) compared to control animals. rhAPC treatment significantly reduced leukocyte adhesion (599±111 n/mm(2)), increased FCD (516±118 cm/cm(2)) and reduced IL-1α levels (2134±937 pg/ml) in the endotoxemic rats. CONCLUSION: APC treatment significantly improves pial microcirculation by reducing leukocyte adhesion and increasing FCD.

Guidelines to the Practice of Anesthesia Revised Edition 2012.

OVERVIEW: The Guidelines to the Practice of Anesthesia Revised Edition 2012 (the guidelines) were prepared by the Canadian Anesthesiologists' Society (CAS), which reserves the right to determine their publication and distribution. Because the guidelines are subject to revision, updated versions are published annually. Whereas previous versions of the guidelines appeared as special supplements to the Canadian Journal of Anesthesia (the Journal), this edition of the guidelines is published within the Journal. This allows for improved archiving and online access to complement the printed version--a new offering for CAS members and Journal subscribers. The Guidelines to the Practice of Anesthesia Revised Edition 2012 supersedes all previously published versions of this document. Although the CAS encourages Canadian anesthesiologists to adhere to its practice guidelines to ensure high-quality patient care, the society cannot guarantee any specific patient outcome. Each anesthesiologist should exercise his or her own professional judgement in determining the proper course of action for any patient's circumstances. The CAS assumes no responsibility or liability for any error or omission arising from the use of any information contained in its Guidelines to the Practice of Anesthesia.

Guidelines to the Practice of Anesthesia: Revised edition 2011.

The Guidelines to the Practice of Anesthesia Revised Edition 2011 (the guidelines) were prepared by the Canadian Anesthesiologists' Society (CAS), which reserves the right to determine their publication and distribution. Because the guidelines are subject to revision, updated versions are published annually. Whereas previous versions of the guidelines appeared as special supplements to the Canadian Journal of Anesthesia (the Journal), this edition of the guidelines is published within the Journal. This allows for improved archiving and online access to complement the printed version-a new offering for CAS members and Journal subscribers. The Guidelines to the Practice of Anesthesia Revised Edition 2011 supersedes all previously published versions of this document. Although the CAS encourages Canadian anesthesiologists to adhere to its practice guidelines to ensure high-quality patient care, the society cannot guarantee any specific patient outcome. Each anesthesiologist should exercise his or her own professional judgement in determining the proper course of action for any patient's circumstances. The CAS assumes no responsibility or liability for any error or omission arising from the use of any information contained in its Guidelines to the Practice of Anesthesia.

Guidelines to the Practice of Anesthesia Revised Edition 2010.

OVERVIEW: The Guidelines to the Practice of Anesthesia Revised Edition 2010 (the guidelines) were prepared by the Canadian Anesthesiologists' Society (CAS), which reserves the right to determine their publication and distribution. Because the guidelines are subject to revision, updated versions are published annually. Whereas previous versions of the guidelines appeared as special supplements to the Canadian Journal of Anesthesia (the Journal), this edition of the guidelines is published within the Journal. This allows for improved archiving and online access to complement the printed version-a new offering for CAS members and Journal subscribers. The Guidelines to the Practice of Anesthesia Revised Edition 2010 supersedes all previously published versions of this document. Although the CAS encourages Canadian anesthesiologists to adhere to its practice guidelines to ensure high-quality patient care, the society cannot guarantee any specific patient outcome. Each anesthesiologist should exercise his or her own professional judgement in determining the proper course of action for any patient's circumstances. The CAS assumes no responsibility or liability for any error or omission arising from the use of any information contained in its Guidelines to the Practice of Anesthesia.