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Mortality risk for elective brain tumor surgery surgery,

Musculoskeletal infection remains a great challenge in orthopedic and trauma surgery. Despite best medical and surgical practice and significant advances in research and development, bone and implant associated infections are still difficult to diagnose, impossible to prevent in all cases and require invasive and debilitating treatment. The development and safe clinical implementation of novel preventative, therapeutic or diagnostic strategies requires the use of animal models of infection, which provide crucial evidence regarding performance, cytocompatibility, biocompatibility, and safety prior to clinical implementation.
Many animal models of musculoskeletal infection have been described in the literature; however, there remains a dearth of fully standardized or universally accepted reference models hindering advancement in the field. The following chapter provides an overview of the animal models available for the study of musculoskeletal infection, the latest advances that are expected to improve them, and some of the most important scientific output achieved using these models.

Autoimmune rheumatic diseases as a group are characterized by common features such as multisystem involvement, polypharmacy, and the presence of comorbidities. Recent large epidemiological studies shed light on their role as risk factors for thromboembolic complications. The pathogenic factors are now better understood. The proposed mechanisms for this increased risk include increased hypercoagulability, lack of inhibitors, and other factors. The group of vasculitis which includes Behçet’s disease, giant cell vasculitis, Takayasu’s arteritis, and ANCA-associated vasculitis deserves special attention. However other diseases such as systemic lupus erythematosus, Sjögren syndrome, scleroderma, rheumatoid and psoriatic arthritis, myositis, and sarcoidosis are also associated with significantly increased risk of thrombosis.

The retained metabolic products in kidney insufficiency are toxic to two main cells connected with blood coagulation, namely, the endothelial cells and the blood platelets. These interact with each other, with leukocytes and with a complex metabolic network involving inflammation, complement activation, coagulation, fibrinolysis, and others. Owing to the unstable nature of kidney insufficiency, the associated coagulation disorders vary from a procoagulant state where endothelial cell injury predominates, to a bleeding disorder where platelet dysfunction supervenes. Amid all that, patients with kidney insufficiency may need anticoagulation either for the commonly associated heart disease, venous thrombosis, antiphospholipid syndrome, etc., for the treatment of certain intrinsic renal disease, or for extracorporeal therapy. This requires a careful benefit/risk balance that can be quantitated by validated scores. As the decision to anticoagulate is made, several practical issues emerge, including the choice of pharmacokinetically compatible agents, their dose in relation to the degree of impairment of kidney function, and potential drug-drug interactions. The decision is confounded by the plethora of currently available anticoagulants, often with superior efficacy, less bleeding tendency, and limited need for monitoring and frequent dose tailoring compared to the traditional heparin and warfarin.