Should All Patients With Pulmonary Hypertension Undergoing Non-Cardiac Surgery Be Managed by Cardiothoracic Fellowship-Trained Anesthesiologists?

Objectives To identify differences in practice patterns and outcomes related to the induction of general anesthesia for patients with pulmonary hypertension (PH) performed by anesthesiologists who have completed a cardiothoracic fellowship (CTA group) vs those who have not (non-CTA group). Design Retrospective study with propensity score matching. Setting Operating room. Participants All adult patients with PH undergoing general anesthesia requiring intubation at a single academic center over 5 years. Interventions Patient baseline characteristics, peri-induction management variables, post-induction mean arterial pressure (MAP), and other outcomes were compared between CTA and non-CTA groups. Methods and main results: Following propensity scoring matching, 402 patients were included in the final model, 100 in the CTA group and 302 in the non-CTA group. Also following matching, only cases of mild to moderate PH without right ventricular dysfunction remained in the analysis. Matched groups were overall statistically similar with respect to baseline characteristics; however, there was a greater incidence of higher ASA class (P = .025) and cardiology and thoracic procedures (P < .001) being managed by the CTA group. No statistical differences were identified in practice patterns or outcomes related to the induction of anesthesia between groups, except for longer hospital length of stay in the CTA group (P = .008). Conclusions These results provide early evidence to suggest the induction of general anesthesia of patients with non-severe PH disease can be comparably managed by either anesthesiologists with or without a cardiothoracic fellowship. However, these findings should be confirmed in a prospective study

Platelet Counts and Postoperative Stroke After Coronary Artery Bypass Grafting Surgery

BACKGROUND: Declining platelet counts may reveal platelet activation and aggregation in a postoperative prothrombotic state. Therefore, we hypothesized that nadir platelet counts after on-pump coronary artery bypass grafting (CABG) surgery are associated with stroke. METHODS: We evaluated 6130 adult CABG surgery patients. Postoperative platelet counts were evaluated as continuous and categorical (mild versus moderate to severe) predictors of stroke. Extended Cox proportional hazard regression analysis with a time-varying covariate for daily minimum postoperative platelet count assessed the association of day-to-day variations in postoperative platelet count with time to stroke. Competing risks proportional hazard regression models examined associations between day-to-day variations in postoperative platelet counts with timing of stroke (early: 0-1 days; delayed: ≥2 days). RESULTS: Median (interquartile range) postoperative nadir platelet counts were 123.0 (98.0-155.0) × 10/L. The incidences of postoperative stroke were 1.09%, 1.50%, and 3.02% for platelet counts >150 × 10/L, 100 to 150 × 10/L, and 150 × 10/L. Importantly, such thrombocytopenia, defined as a time-varying covariate, was significantly associated with delayed (≥2 days after surgery; adjusted HR, 2.83; 95% CI, 1.48-5.41; P= .0017) but not early postoperative stroke. CONCLUSIONS: Our findings suggest an independent association between moderate to severe postoperative thrombocytopenia and postoperative stroke, and timing of stroke after CABG surgery

Altered aquaporin 9 expression and localization in human hepatocellular carcinoma

AbstractBackgroundIn addition to the biochemical components secreted in bile, aquaporin (AQP) water channels exist in hepatocyte membranes to form conduits for water movement between the sinusoid and the bile canaliculus. The aim of the current study was to analyse AQP 9 expression and localization in human hepatocellular carcinoma (HCC) and non-tumourigenic liver (NTL) tissue from patients undergoing hepatic resection.MethodsArchived tissue from 17 patients was sectioned and analysis performed using an antibody raised against AQP 9. Slides were blind-scored to determine AQP 9 distribution within HCC and NTL tissue.ResultsAquaporin 9 was predominantly expressed in the membranes of hepatocytes and demonstrated zonal distribution relative to hepatic sinusoid structure in normal liver. In HCC arising in the absence of cirrhosis AQP 9 remained membrane-localized with zonal distribution in the majority of NTL. By contrast, AQP 9 expression was significantly decreased in the HCC mass vs. pair-matched NTL. In HCC in the presence of cirrhosis, NTL was characterized by extensive AQP 9 staining in the membrane in the absence of zonal distribution and AQP 9 staining in NTL was significantly greater than that observed in the tumour mass.ConclusionsThese data demonstrate that human HCC is characterized by altered AQP 9 expression and AQP 9 localization in the NTL mass is dependent on underlying liver pathology. Given the central role of AQPs in normal liver function and the potential role of AQPs during transformation and progression, these data may prove valuable in future diagnostic and/or therapeutic strategies