Bone cement implantation syndrome (BCIS) is a potentially fatal complication of orthopedic surgeries that use cement. The symptoms of BCIS occur primarily during femoral fracture repairs, but this complication has been reported in a wide variety of cemented procedures. Clinical presentation of this syndrome begins as a cascade with hypoxia and hypotension; if it is not reversed, it ends with right‐sided heart failure and cardiac arrest. This syndrome usually occurs at cementation, prosthesis insertion, joint reduction, or tourniquet deflation, and should be treated with aggressive resuscitation and supportive care. This article provides a comprehensive explanation of bone cement, the identification and management of BCIS, and the roles of the perioperative team in the event of cardiopulmonary collapse. It includes a case study that can be used as an educational tool for simulation, mock drills, or staff meetings; it also may be used as a framework for creating policies.
Drug-induced liver injury (DILI) is common and nearly all classes of medications can cause liver disease. Most cases of DILI are benign, and improve after drug withdrawal. It is important to recognize and remove the offending agent as quickly as possible to prevent the progression to chronic liver disease and/or acute liver failure. There are no definite risk factors for DILI, but preexisting liver disease and genetic susceptibility may predispose certain individuals. Although most patients have clinical symptoms that are identical to other liver diseases, some patients may present with symptoms of systemic hypersensitivity. Treatment of drug and herbal-induced liver injury consists of rapid drug discontinuation and supportive care targeted to alleviate unwanted symptoms. KeywordsDrug-induced liver injury (DILI); drug-induced hepatitis; drug-induced cholestasis; acetaminophen; vanishing bile duct syndrome; herbal toxicity Adverse drug reactions are an important cause of liver injury that may require discontinuation of the offending agent, hospitalization, or even liver transplantation. 1 Indeed, drug-induced hepatotoxicity is the most frequent cause of acute liver failure in US. 2 Because the liver is responsible for concentrating and metabolizing a majority of medications, it is a prime target for medication-induced damage. Among hepatotoxic drugs, acetaminophen (paracetamol) is the most often studied. However, a broad range of different pharmacological agents can induce liver damage, including anesthetics, anticancer drugs, antibiotics, antituberculosis agents, antiretrovirals, and cardiac medications. In addition, a plethora of traditional medical therapies and herbal remedies may also be hepatotoxic.Depending on the duration of injury and the histological location of damage, drug-induced liver injury (DILI) is categorized as acute or chronic, and either as hepatitis, cholestatic, or a mixed pattern of injury. The hepatitis pattern is characterized by hepatocyte necrosis and is associated with a poor prognosis. There are three types of acute cholestatic drug-induced injury: bland cholestasis is the result of abnormal biliary secretion, and is not accompanied by significant hepatocellular damage; cholestatic hepatitis (mixed type) refers to cholestasis with concomitant hepatic parenchymal damage; and the third form of acute cholestasis is
Valproic acid (VPA) is a medication used to treat multiple neuroscience conditions. It is an inexpensive and useful medication, with a low incidence of adverse drug events. Nonetheless, optimal clinical outcomes require that a series of screening and laboratory steps be followed before the initiation of VPA therapy. An additional aspect of pharmacovigilance is to recognize clinical patterns signaling genetic traits that preclude VPA, background of the black box warnings, targeted assessments, and laboratory monitoring indicated while on VPA. The intention of this article is to provide a focused summary of published information clinically relevant to prescribing and monitoring these patients.
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