In the last few decades, epidural administration of various drugs has gained popularity and widespread clinical acceptance. Epidural administration of local anesthetics and opioids has been considered “state of the art” in acute pain management (thoracic and major abdominal surgery, labor). Its advantage is that it yields profound, long-lasting, dose-dependent analgesia, leaving other sensory and motor functions intact. It facilitates early patient mobilization and ambulation and therefore reduces the risk of postoperative thromboembolism and respiratory complications. The increment in the elderly population caused an increase in musculoskeletal and spine diseases and thus, epidural steroid injections have become highly effective for chronic pain treatment. There are many factors that have an impact on drug physiology and pharmacology in the epidural space and, therefore, can modify epidural anesthesia or the expected effect of another medication. This chapter provides insight into this complex and comprehensive topic to demonstrate a predictable pattern that can provide a safe and accurate guide to clinical practice.

Tumour lysis syndrome (TLS) is a group of pathophysiological processes caused by rapid degradation of tumour cells with subsequent release of intracellular contents into the extracellular space. It is characterized by the development of systemic metabolic disturbances with or without clinical manifestations. The process usually occurs in highly proliferative, large tumours after induction of cytotoxic therapy. Rarely, however, spontaneous TLS can develop, as well as signs of multiorgan failure triggered by an excessive metabolic load and sterile inflammation. The combination of the aforementioned is thus quite unique. Here, we present a 63-year-old male in which spontaneous TLS was accompanied with acute liver failure and delineated underlying nonHodgkin lymphoma. Initial laboratory findings included hyperkalaemia, hyperphosphataemia, hypocalcaemia, uraemia, and increased creatinine levels indicating the onset of TLS with acute kidney injury. Moreover, the patient showed signs of jaundice, coagulopathy, and hepatic encephalopathy. Development of TLS with multiorgan failure prompted rapid initiation of critical care management, including vigorous intravenous fluid therapy, allopurinol treatment, high flow continuous venovenous haemodiafiltration, and commencement of chemotherapy. The case highlights the possibility of TLS as a differential diagnosis in patients presenting with multiorgan failure and the importance of early detection of this potentially challenging and fatal diagnosis.