Septic embolism is a relatively common and potentially severe complication of infective endocarditis (IE). Septic emboli (SE), most often described as consisting of a combination of thrombus and infectious material—either bacterial or fungal—can be caused by hematogenous spread from virtually any anatomic site; however, it most commonly originates from cardiac valves. During the past two decades there has been a confluence of various risk factors that, both alone and in combination, led to greater incidence of both IE and SE, including increasing population age, greater use of prosthetic valves, implantation of various intracardiac devices, escalating intravenous drug use, and the high incidence of healthcare associated infections with antibiotic resistant microorganisms. From a clinical standpoint, SE can present at any time during the course of IE and may even be the initial presenting sign. SE may affect virtually any location in the human body, but some organs (e.g., liver, spleen, brain) and anatomic regions (e.g., lower extremity) tend to be more frequently involved. The most important aspect of management involves prompt recognition and proactive therapeutic approach. Given the broad spectrum of clinical presentations, symptoms and complications, SE can be challenging to diagnose and treat. Following the identification of SE, appropriate antibiotic coverage should be immediately instituted followed by supportive and/or interventional management, depending on the severity of presentation and the associated complications. In this chapter we explore the pathophysiology, anatomic origins, diagnostic tools, therapeutic measures, and new developments in SE, focusing predominantly on bacterial infections of cardiac origin.
Part of the book: Advanced Concepts in Endocarditis
Neurogenic shock is a state characterized by hypotension, bradycardia, and other evidence of autonomic dysfunction. The most common cause is acute spinal cord injury (SCI), which will be the subject of our focus. Because the typical autonomic reflexes may be either abolished or dysregulated, appropriate treatment requires an understanding of the neuroanatomic substrate for the change. In this chapter, we will explore the root cause for neurogenic shock, differentiating it from spinal shock, and discuss those patients at risk and generally accepted treatment paradigms. The timeframe for manifestation of neurogenic shock is variable and it can quickly progress to cause secondary injury or death, so appropriate monitoring requires a high level of suspicion and diligence.
Part of the book: Clinical Management of Shock