Perioperative Allogeneic Blood Transfusion Is Associated With Surgical Site Infection After Abdominoperineal Resection—a Space for the Implementation of Patient Blood Management Strategies

Allogeneic blood transfusion (ABT) has been reported as a major risk factor for surgical site infection (SSI) in patients undergoing colorectal surgery. However, the association of ABT with SSI in patients undergoing abdominoperineal resection (APR) and total pelvic exenteration (TPE) still remains to be evaluated. Here, we aim to elucidate this association. The medical records of all patients undergoing APR and TPE at our institution in the period between January 2000 and December 2012 were reviewed. Patients without SSI (no SSI group) were compared with patients who developed SSI (SSI group), in terms of clinicopathologic features, including ABT. In addition, data for 262 patients who underwent transabdominal rectal resection at our institution in the same period were also enrolled, and their data on differential leukocyte counts were evaluated. Multivariate analysis showed that intraoperative transfusion was an independent predictive factor for SSI after APR and TPE (P = 0.004). In addition, the first–operative day lymphocyte count of patients undergoing APR, TPE, and transabdominal rectal resection was significantly higher in nontransfusion patients compared with transfusion ones (P = 0.026). ABT in the perioperative period of APR and TPE may have an important immunomodulatory effect, leading to an increased incidence of SSI. This fact should be carefully considered, and efforts to avoid allogeneic blood exposure while still achieving adequate patient blood management would be very important for patients undergoing APR and TPE as well.Key words: Colorectal cancer, Abdominoperineal resection, Surgical site infection, Allogeneic blood transfusion, Patient blood managementPostoperative surgical site infection (SSI) is one of the most frequent complications associated with various surgical procedures, and it results in adverse outcomes, including longer hospital stay, higher health care costs, and increased surgical mortality.¹ It is one of the most frequent nosocomial complications, accounting for almost one fifth of all health care–associated infections.² Colon surgery and rectal surgery are associated with higher SSI rates compared with most other abdominal procedures, with 5% to 25% of colon and rectal surgery patients developing incisional and organ/space SSI.^3–5 Moreover, the incidence of overall SSI was reported to be higher in rectal surgery patients (17%–28%) than in colonic surgery patients (9%–23%),^3,5,6 with especially higher overall SSI rates observed in patients undergoing abdominoperineal resection (APR; 12%–51%).^7–9 These are attributed to the high infection rates of the perineal wound, reported to be as high as 21%.¹⁰ Thus, the incidence of SSI associated with APR should be the highest among the various abdominal operative procedures.Various risk factors for postoperative SSI in colorectal surgery were reported previously. Open surgery,^10–12 perioperative allogeneic blood transfusion (ABT),^4,10,12 and prolonged operation time^4,9 have been found to be risk factors for SSI in a number of studies. Although several preceding reports have investigated the risk factors for SSI associated with APR, the reported independent risk factors varied among the studies. Although a number of studies have reported on the role of ABT as a strong risk factor for incisional SSI in colorectal surgery,^13,14 only one study has investigated on its relevance to the onset of incisional SSI after APR procedure; but this study failed to demonstrate a significant association. Presently, therefore, the role of ABT as a potential risk factor for incisional SSI in APR remains to be elucidated, and doing so will be very important for the implementation of measures to achieve patient blood management in this group of patients.In this study, we aimed to elucidate the risk factors for SSI in patients receiving APR, especially focusing on ABT.     

Conjugated bile salts regulate turnover of rat intestinal brush border membrane hydrolases

The mechanisms whereby the conjugated bile salts regulate the activities of the brush border membrane hydrolases and its physiological significance were investigated in rat small intestine, and comparisons were made with the action of pancreatic protease. Rat brush border membrane proteins were metabolically labeled with [³⁵S]methionine, and isolated brush border membrane was incubated with taurocholate or pancreatic elastase. The activity of solubilized hydrolases was assayed and the molecular forms of the hydrolases were examined by SDS-PAGE. The activity and protein bands of alkaline phosphatase and sucrase-isomaltase were solubilized by taurocholate, while alkaline phosphatase was not solubilized by elastase. Solubilized sucrase-isomaltase molecules were proteolytically degraded by elastase, whereas the intact molecule of sucrase-isomaltase was solubilized by taurocholate. Next the physiological role of bile salts in brush border membrane hydrolase turnover were investigated using metabolic labeling of brush border membrane hydrolase and immunoprecipitation in biliary diversion rats. After three days of biliary diversion, a significant increase in alkaline phosphatase activity was observed. Although synthesis of alkaline phosphatase in biliary diversion rats was similar to that observed in control rats, biliary diversion rats showed 1.5-fold slower turnover of alkaline phosphatase when compared with control rats. These results suggest that conjugated bile salts in the intestinal lumen may cause a rapid turnover of brush border membrane hydrolases, which may be increased by the enhanced enzyme degradation. The mechanisms for the enhanced degradation appeared to be solubilization of hydrolases caused by the detergent activity of bile salts. Therefore, conjugated bile salts may play an important physiological role in the regulation of expression of the protease-resistant enzymes such as alkaline phosphatase.     

A case of bullous pemphigoid associated with Pneumocystis pneumonia and Cytomegalovirus pneumonia]

A 68-year-old man was admitted to our hospital presenting cutaneous pruritic lesions consisting of tense blisters with serous content on his arms and legs. Histological findings of skin biopsy confirmed a diagnosis of bullous pemphigoid in March 2005. After 10 weeks of prednisone therapy for bullous pemphigoid, he presented with increasing breathlessness and high fever. He was admitted to our hospital because of severe hypoxemia on May 29, 2005, and mechanical ventilation was started from the first hospital day. Chest computed tomography showed marked ground-glass opacities in both lungs. The levels of beta-D glucan and KL-6 in his sera were elevated. We suspected Pneumocystis pneumonia and Cytomegalovirus pneumonia. Under mechanical ventilation, he received steroid pulse therapy, and sulfamethoxazole-trimethoprim and ganciclovir. A polymerase chain reaction assay of bronchoalveolar lavage fluid showed Pneumocysitis DNA and Cytomegalovirus DNA. On the 12th hospital day, he was weaned from mechanical ventilation. Follow-up chest computed tomography showed marked resolution of diffuse ground-glass opacity in both lungs. We need to consider the development of Pneumocystis pneumonia and Cytomegalovirus pneumonia during steroid therapy for bullous pemphigoid.     

Role of platelets in chronic liver disease and acute liver injury

Platelets contain not only hemostatic factors but also many growth factors that play important roles in wound healing and tissue repair. Platelets have already been used for the promotion of tissue regeneration in the clinical setting, such as dental implantation and plastic surgery. Thrombocytopenia, which is frequently found in patients with chronic liver disease and cirrhosis, is due to various causes such as decreased thrombopoietin production and accelerated platelet destruction caused by hypersplenism. However, the relationship between thrombocytopenia and hepatic pathogenesis and the role of platelets in chronic liver disease are poorly understood. In acute liver injury, it is reported that platelets are recruited to the liver and contribute to liver damage by promoting the induction of chemotactic factors and the accumulation of leukocytes in the liver, whereas platelets or mediators released by platelets can have a protective effect against liver injury. In this review, we highlight the recent accumulated knowledge concerning the role of platelets in chronic liver disease and acute liver injury.     

Plasma Exchange Therapy to Reduce Mortality in Japanese Patients With Diffuse Alveolar Hemorrhage and Microscopic Polyangiitis

Diffuse alveolar hemorrhage (DAH) is well known as a serious complication of microscopic polyangiitis (MPA). We examined the effectiveness of plasma exchange (PLEX) therapy to reduce mortality in Japanese DAH patients with MPA. This retrospective, double‐center, observational cohort study included 20 DAH patients with MPA who were admitted to Juntendo University Hospital or Juntendo Koto Geriatric Medical Center between April 1998 and March 2018. The primary outcome was non–disease‐specific mortality. The 1‐year survival rate of patients with PLEX therapy (N = 4) was higher than that of patients with conventional therapy (N = 16, 75% and 13%, respectively, P = 0.037). Higher values of the 1996 Five‐Factor Score (FFS) and 2009 FFS were associated with increased mortality, with hazard ratios of 2.29 (P = 0.040) and 2.41 (P = 0.043), respectively, by Cox univariate analysis. We investigated PLEX therapy for reducing mortality in DAH patients with MPA, and the 1996 FFS and 2009 FFS were both independent prognostic factors.