Prolonged course of eravacycline leading to acute pancreatitis.

Eravacycline is the newest member of the broad-spectrum class of tetracycline antimicrobials. Pancreatitis has been previously associated with the tetracycline class of antibiotics, but, to our knowledge, we believe that this is the first reported case of eravacycline-induced pancreatitis. We describe a 46-year-old male who received eravacycline for treatment of a perirectal abscess. While the patient had slightly elevated lipase levels at baseline post-cardiopulmonary arrest, he developed abdominal pain and a further increase in lipase levels following 10 days of eravacycline, consistent with pancreatitis. Based on the Naranjo adverse drug reaction probability scale, eravacycline was the probable etiology of acute pancreatitis given improvement immediately after discontinuation. Clinicians should be aware of this potential adverse effect of eravacycline and should not initiate eravacycline in those with risk factors for acute pancreatic injury. However, acute pancreatitis should be suspected in all patients complaining of symptoms followed by immediate discontinuation of eravacycline.

Assessing clinical cure of empirical piperacillin/tazobactam for ESBL urinary tract infections (ACCEPT-UTI).

Background: Data are limited regarding use of piperacillin/tazobactam for ESBL urinary tract infections (UTIs). The objective of this study was to compare clinical outcomes of patients treated empirically with piperacillin/tazobactam versus carbapenems for ESBL UTIs. Methods: This retrospective, observational, propensity score-matched study evaluated adults with an ESBL on urine culture. Patients who had UTI symptoms or leukocytosis, and who received a carbapenem or piperacillin/tazobactam empirically for at least 48 h were included. The primary outcome was clinical success within 48 h, defined as resolution of temperature (36-38°C), resolution of symptoms or leukocytosis (WBC <12 × 103/µL) in the absence of documented symptoms, and the absence of readmission for an ESBL UTI within 6 months. Secondary outcomes included time to clinical resolution, hospital length of stay, and in-hospital and 30 day all-cause mortality. Results: Overall, 223 patients were included in the full cohort and 200 patients in the matched cohort (piperacillin/tazobactam = 100, carbapenem = 100). Baseline characteristics were similar between the groups. There was no difference in the primary outcome of clinical success between the carbapenem and piperacillin/tazobactam groups (58% versus 56%, respectively; P = 0.76). Additionally, there was no difference in median (IQR) time to clinical resolution [38.9 h (21.5, 50.9 h) versus 40.3 h (27.4, 57.5 h); P = 0.37], in-hospital all-cause mortality (3% versus 3%; P = 1.00), or 30 day all-cause mortality (4% versus 2%; P = 0.68) between the carbapenem and piperacillin/tazobactam groups, respectively. Conclusions: There was no significant difference in clinical success for patients treated empirically with piperacillin/tazobactam compared with carbapenems for ESBL UTIs.

Management of noncytotoxic extravasation injuries: A focused update on medications, treatment strategies, and peripheral administration of vasopressors and hypertonic saline.

Extravasation is the leakage of intravenous solutions into surrounding tissues, which can be influenced by drug properties, infusion techniques, and patient-related risk factors. Although peripheral administration of vesicants may increase the risk of extravasation injuries, the time and resources required for central venous catheter placement may delay administration of time-sensitive therapies. Recent literature gathered from the growing use of peripheral vasopressors and hypertonic sodium suggests low risk of harm for initiating these emergent therapies peripherally, which may prevent delays and improve patient outcomes. Physiochemical causes of tissue injury include vasoconstriction, pH-mediated, osmolar-mediated, and cytotoxic mechanisms of extravasation injuries. Acidic agents, such as promethazine, amiodarone, and vancomycin, may cause edema, sloughing, and necrosis secondary to cellular desiccation. Alternatively, basic agents, such as phenytoin and acyclovir, may be more caustic due to deeper tissue penetration of the dissociated hydroxide ions. Osmotically active agents cause cellular damage as a result of osmotic shifts across cellular membranes in addition to agent-specific toxicities, such as calcium-induced vasoconstriction and calcifications or arginine-induced leakage of potassium causing apoptosis. A new category has been proposed to identify absorption-refractory mechanisms of injury in which agents such as propofol and lipids may persist in the extravasated space and cause necrosis or compartment syndrome. Pharmacological antidotes may be useful in select extravasations but requires prompt recognition and frequently complex administration strategies. Historically, intradermal phentolamine has been the preferred agent for vasopressor extravasations, but frequent supply shortages have led to the emergence of terbutaline, a ß2 -agonist, as an acceptable alternative treatment option. For hyperosmolar and pH-related mechanisms of injuries, hyaluronidase is most commonly used to facilitate absorption and dispersion of injected agents. However, extravasation management is largely supportive and requires a protocolized multidisciplinary approach for early detection, treatment, and timely surgical referral when required to minimize adverse events.