Warshaw Technique in Laparoscopic Spleen-Preserving Distal Pancreatectomy: Surgical Strategy and Late Outcomes of Splenic Preservation.

Laparoscopic spleen-preserving distal pancreatectomy (LSPDP) can be accomplished with either the preservation or the resection of splenic vessels; the latter is also known as Warshaw technique. Our study is designed to investigate the operation selection strategy when proceeding LSPDP and to evaluate the long-term outcomes of patients undergoing Warshaw surgery. The medical records and follow-up data of patients who underwent LSPDP in Qilu Hospital, Shandong University, were reviewed retrospectively. A total of thirty-five patients were involved in this study, including 17 cases of patients who were treated with Warshaw procedure (WT) while the other 18 cases had splenic vessels preserved (SVP). Compared with the SVP group, the operative time and intraoperative blood loss in WT group were improved significantly. The incidence of early postoperative splenic infarction was higher in WT group. However, there was no report of splenic abscess or second operation. Follow-up data confirmed that there was no significant difference in spleen phagocytosis and immune function compared with normal healthy population. Our study confirms that LSPDP-Warshaw procedure is a safe and efficient treatment for the benign or low grade malignant tumors in distal pancreas in selected patients. The long-term spleen function is normal after Warshaw procedure. Preoperative assessment and intraoperative exploration are recommended for the selection of operation approaches.

Treatment of large avulsion injury in perianal, sacral, and perineal regions by island flaps or skin graft combined with vacuum assisted closure.

BACKGROUND: Traumatic avulsion injuries to the anus, although uncommon, can result in serious complications and even death. Management of anal avulsion injuries remains controversial and challenging. This study aimed to investigate the clinical effects of treating large skin and subcutaneous tissue avulsion injuries in the perianal, sacral, and perineal regions with island flaps or skin graft combined with vacuum assisted closure. METHODS: Island flaps or skin graft combined with vacuum assisted closure, diverting ileostomy, the rectum packed with double-lumen tubes around Vaseline gauze, negative pressure drainage with continuous distal washing, wounds with skin grafting as well as specialized treatment were performed. RESULTS: The injuries healed in all patients. Six cases had incomplete perianal avulsion without wound infection. Wound infection was seen in four cases with annular perianal avulsion and was controlled, and the separated prowl lacuna was closed. The survival rate in 10 patients who underwent skin grafting was higher than 90%. No anal stenosis was observed after surgery, and ileostomy closure was performed at 3 months (six cases) and 6 months (four cases) after surgery, respectively. CONCLUSIONS: Covering a wound with an island flap or skin graft combined with vacuum assisted closure is successful in solving technical problems, protects the function of the anus and rapidly seals the wound at the same time.

Assessment of immune cells and function of the residual spleen after subtotal splenectomy due to splenomegaly in cirrhotic patients.

BACKGROUND: The spleen is thought to be central in regulating the immune system, a metabolic asset involved in endocrine function. Overwhelming postsplenectomy infection leads to a mortality rate of up to 50%. However, there is still controversy on performing subtotal splenectomy as treatment of splenomegaly due to portal hypertension in cirrhotic patients. In the present study, immunocytes and the indexes of splenic size, hemodynamics, hematology and immunology in the residual spleen were analyzed to support subtotal splenectomy due to splenomegaly. RESULTS: In residual spleen, T lymphocytes mainly were focal aggregation in the periarterial lymphatic sheath. While B lymphocytes densely distributed in splenic corpuscle. In red pulp, macrophages were equally distributed in the xsplenic cord and adhered to the wall of splenic sinus with high density. The number of unit area T and B lymphocytes of splenic corpuscle and marginal zone as well as macrophages of red pulp were obviously increased in the residual spleen, while the number of macrophages didn't be changed among the three groups in white pulp. While there were some beneficial changes (i.e., Counts of platelet and leucocyte as well as serum proportion of CD3+ T cells, CD4+ T cells, CD8+ T cells were increased markedly; serum levels of M-CSF and GM-CSF were decreased significantly; The proportion of granulocyte, erythrocyte, megakaryocyte in bone marrow were changed obviously; But serum IgA, IgM, IgG, Tuftsin level, there was no significant difference; splenic artery flow volume, portal venous diameter and portal venous flow volume, a significant difference was observed in residual spleen) in the clinical indices. CONCLUSION: After subtotal splenectomy with splenomegaly due to portal hypertension in cirrhotic patients, the number of unit area T and B lymphocytes, and MØ in red pulp of residual spleen increased significantly. However, whether increase of T, B lymphocytes and MØs in residual splenic tissue can enhance the immune function of the spleen, still need further research to confirm.

Mechanistic insights of sulfur mustard-induced acute tracheal injury in rats.

Sulfur mustard (SM) is believed to be a major threat to civilian populations because of the persistent asymmetric threat by nonstate actors, such as terrorist groups, the ease of synthesis and handling, and the risk of theft from stockpiles. The purpose of this study was to establish mechanisms of acute tracheal injury in rats induced by SM using histopathologic, immunohistochemical, and biochemical parameters. Male rats (Sprague-Dawley) were anesthetized, intratracheally intubated, and exposed to 2 mg/kg of SM. Animals were euthanized 6-, 24-, 48-, and 72-hour postexposure, and intracavitary blood samples from the heart and tracheal tissues were collected. Exposure of rats to SM resulted in rapid tracheal injury, including tracheal epithelial cell shedding, focal ulceration, and abundant lymphocyte invasion of the submucosa. There was also evidence of a large number of apoptotic cells in the epithelium and submucosa, the serum levels of tumor necrosis factor α, interleukin 1ß (IL) 1ß, IL-6, and γ-glutamyl transferase peaked at 24 hours, and the serum levels of lactate dehydrogenase, glutathione peroxidase, and thiobarbituric acid reactive substance peaked at 6 hours. The SM exposure also resulted in a loss of the cellular membrane, leakage of cytoplasm, fuzzy mitochondrial cristae, medullary changes in ciliated and goblet cells, and the nuclear chromatin appeared marginated in basal cells and fibroblasts. The results in the propylene glycol group were the same as the control group. These data demonstrated the histologic changes, inflammatory reactions, apoptosis, oxidative stress, and DNA damage following SM (2 mg/kg)-induced acute tracheal injury; the severity of changes was time dependent.

Assessment of the infiltration of inflammatory cells in the walls of thrombotic varicose veins.

The purpose of this study is to describe the infiltration of mast cells as well as T and B cells in the walls of thrombotic varicose great saphenous veins. Sections were obtained from venous segments of patients with varicose veins and stained with toluidine blue for mast cells, while immunohistochemistry for T cells (using CD45RO antibody) and B cells (CD20) was analyzed using light microscopy after staining. The number of mast cells, T, and B cells observed in thrombotic varicose veins was 1.925 ± 1.203, 72.038 ± 34.707, and 19.519 ± 9.899, respectively. In varicose veins, the corresponding values were 0.265 ± 0.099, 0.600 ± 0.432, and 0.488 ± 0.400. Significantly higher number of mast cells, T cells, and B cells were observed in thrombotic varicose veins compared with control veins. A significant difference was not observed between the varicose group and control group. Thrombi in varicose veins can induce infiltration of mast cells, T cells, and B cells, which may be involved in the remodeling of venous walls.