Cognitive Aids for the Management of Thoracic Anesthesia Emergencies: Consensus Guidelines on Behalf of a Canadian Thoracic Taskforce.

A cognitive aid is a tool used to help people accurately and efficiently perform actions. Similarly themed cognitive aids may be collated into a manual to provide relevant information for a specific context (eg, operating room emergencies). Expert content and design are paramount to facilitate the utility of a cognitive aid, especially during a crisis when accessible memory may be limited and distractions may impair task completion. A cognitive aid does not represent a rigid approach to problem-solving or a replacement for decision-making. Successful cognitive aid implementation requires dedicated training, access, and culture integration. Here the authors present a set of evidence-based cognitive aids for thoracic anesthesia emergencies developed by a Canadian thoracic taskforce.

Epidural analgesia? A prospective analysis of perioperative coagulation in cytoreductive surgery and hyperthermic intraperitoneal chemotherapy.

BACKGROUND: Cytoreductive surgery (CRS) and heated intraperitoneal chemotherapy (HIPEC) is beneficial in peritoneal carcinomatosis. Epidurals provide excellent pain relief for laparotomies. Coagulopathy (platelet count <100 × 109/L, INR>1.5 or PTT >45) occurs with CRS and HIPEC, increasing risk for bleeding complications with epidurals. This prospective study characterizes clot kinetics with thromboelastography (TEG) to determine suitability for epidural analgesia. METHODS: After Research Ethics approval, thirty consented patients had blood collected. Primary data collected included TEG and conventional coagulation measures (platelets, PTT and INR). Secondary data collected included demographics, disease, surgical, intraoperative factors and complications from epidural placement. RESULTS: Of 30 patients analyzed, two had incomplete data. Four developed abnormal coagulation between the second and fifth post-operative day. For all patients, TEG values remained normal. Postoperative INR was elevated until day 3 (all INR < 1.5). 17 patients received epidural analgesia, 3 demonstrated abnormal conventional coagulopathic criteria despite normal TEG. CONCLUSIONS: In this study CRS and HIPEC do not contribute to the conventional definition of clinical coagulopathy. Clot kinetics indicate that epidural catheters may be recommended for post-operative analgesia.

Hypotension in the Right Lateral Position Secondary to Inferior Vena Cava Abnormality.

Surgical positioning is accompanied by numerous anesthetic considerations, particularly its potential effects on the cardiovascular, respiratory, and nervous systems. Clinical studies have shown that lateral positioning does not affect hemodynamics; however, with the addition of trunk flexion, there is a decrease in cardiac output, which may be secondary to caval compression. In this report, we describe a unique case of hypotension that arose in a patient positioned only in the right lateral decubitus position with flexion and that was exacerbated by an abnormally narrow inferior vena cava.

Role of the TLR signaling molecule TRIF in ß-cell function and glucose homeostasis.

Type 2 diabetes is a metabolic and inflammatory disease characterized by deteriorating islet function and increased levels of inflammatory cytokines. The inflammatory milieu induced in type 2 diabetes exacerbates islet dysfunction and insulin resistance, and therapies that target inflammation can improve glycemic control in patients with type 2 diabetes. Inflammation in type 2 diabetes may be the result of the stimulation of Toll-like receptors (TLRs), one of the many mediators of inflammation. TLRs can be activated by both exogenous and endogenous ligands, and are responsible for activating NFκB and interferon- inducible inflammatory gene expression. We examined the role of the TIR-domain containing adaptor-inducing interferon-ß (TRIF or TICAM-1), a major signaling molecule for TLR3 and TLR4, in b-cell function and glucose homeostasis by examining mice lacking TRIF (Trif⁻(/)⁻), TLR3 (Tlr3⁻(/)⁻) or TLR4 (Tlr4⁻(/)⁻). Male, 10-week old Trif⁻(/)⁻ mice exhibit a moderate but significant increase in fasting blood glucose compared to C57BL/6 controls (12.0 ± 0.9 vs. 9.7 ± 0.4 mM; p < 0.05) as well as impaired glucose tolerance revealed by IPGTT (AUC: 2850 ± 236 vs. 2050 ± 108; p < 0.005) whereas Tlr3⁻(/)⁻ and Tlr4⁻(/)⁻ mice have normal glucose tolerance. Interestingly, Trif⁻(/)⁻ mice have normal insulin sensitivity yet have increased plasma insulin levels (180 ± 22 vs. 89 ± 24 pM; p < 0.05). Islets isolated from Trif⁻(/)⁻ mice have impaired glucose-stimulated insulin secretion, with a diminished first-phase insulin response to glucose. Immunohistological analysis revealed that age-matched Trif⁻(/)⁻ and control mice have normal islet morphology, although Trif⁻(/)⁻ mice have increased b-cell mass (3.5 ± 0.9 vs. 1.7 ± 0.2 mg; p < 0.05). In summary, mice lacking TRIF have hyperglycemia associated with b-cell dysfunction that may be partly compensated for by increased b-cell mass. These studies suggest a role for TLR signaling in glucose homeostasis, and raise the possibility that TRIF signaling is required for normal b-cell function.

Islet allograft rejection is independent of toll-like receptor signaling in mice.

BACKGROUND: Islet transplantation is a promising therapy for type 1 diabetes; however, most islet grafts fail within 5 years. Innate immunity has been suggested to play a role in islet allograft rejection, potentially mediated by toll-like receptors (TLRs), a class of innate immune receptors. Lack of TLR4, in particular, has been reported to improve allograft survival. Therefore, we hypothesized that TLRs may be involved in islet allograft rejection, and that deletion of TLR4 may improve islet graft survival. METHODS: Islets were isolated from C57BL/10ScNJ (Tlr4(-/-)) and C57BL/10 (wild-type [WT]) animals and transplanted into Balb/cJ recipients with streptozotocin-induced diabetes. Blood glucose levels were used to determine graft viability and immunostaining to assess graft morphology and immune cell infiltration. The roles of the TLR4 adaptor molecules MyD88 and TLR adaptor molecule 1 (Ticam-1) were assessed using islets isolated from mice lacking MyD88 (MyD88(-/-)), Ticam-1 (Ticam-1(-/-)), or the combined double knockout (MyD88(-/-)/Ticam-1(-/-)). RESULTS: Contrary to our hypothesis, Tlr4(-/-) and WT islet allografts had similar failure rates; grafts failed at 23.2+/-1.2 and 24.5+/-1.5 days posttransplant, respectively (P=NS). Syngeneic grafts of Tlr4(-/-) and WT islets maintained normoglycemia for up to 10 weeks posttransplant, indicating that failure of Tlr4(-/-) islet allografts could not be attributed to an intrinsic defect in Tlr4(-/-) islets. Similarly, islet allotransplants from MyD88(-/-), Ticam-1(-/-), and MyD88(-/-)/Ticam-1(-/-) donors did not have improved allograft survival compared with WT controls. CONCLUSIONS: These findings indicate that islet allograft rejection in mice is independent of TLR4 and the TLR adaptor molecules MyD88 and Ticam-1, speaking against an essential role for TLR signaling in islet allograft rejection.