No abstract

A majority of patients with severe sepsis and septic shock are first evaluated in the emergency department (ED). Methods such as screening tools have proven advantageous in earlier identification, allowing for timely initiation of treatment. Delay in symptom presentation and ED overcrowding contribute to deferment of sepsis bundle components and admission. To examine the impact of time from ED arrival to inpatient admission on mortality and length of stay (LOS) in patients with severe sepsis or septic shock. A retrospective analysis of adult patients with severe sepsis or septic shock was completed for those presenting between January 2013 and December 2014. Patients were dichotomized on the basis of the length of time from completed triage in the ED to intensive care unit (ICU) admission (at less than 6 hr and at 6 hr or more). Of the 294 patients screened, 172 patients (58.5%) met inclusion criteria (n = 70 cases at less than 6 hr; n = 102 at 6 hr or more). Mean wait time from ED arrival to ICU admission was 470.7 ± 333.9 min (range = 84-2,390 min). Groups were similar in baseline, disease severity, and bundle characteristics. There were no differences in the less than 6-hr group compared with the 6-hr-or-more group in rates of 30-day mortality (37.1% vs. 32.4%; p = 0.52), as well as in-hospital (27.1% vs. 23.5%; p = 0.59) or 90-day mortality (42.9% vs. 34.3%; p = 0.26). There were also no differences in hospital or ICU LOS. Timing of transfer from the ED to the ICU was not found to impact mortality or LOS. These results suggest that the ED can provide similar sepsis care to that in the ICU when transfer is delayed in patients with sepsis.

Pneumonia is common in the intensive care unit (ICU), infecting 27% of all critically ill patients. Given the high prevalence of this disease state in the ICU, optimizing antimicrobial therapy while minimizing toxicities is of utmost importance. Inappropriate antimicrobial use can increase the risk of antimicrobial resistance, Clostridiodes difficile infection, allergic reaction, and other complications from antimicrobial use (e.g., QTc prolongation, thrombocytopenia). This review article aims to discuss methods to optimize antimicrobial treatment in patients with pneumonia, including the following: procalcitonin use, utilization of methicillin-resistant Staphylococcus aureus nares testing to determine need for vancomycin therapy, utilization of the Biofire® FilmArray® pneumonia polymerase chain reaction (PCR), and microbiology reporting techniques.

Incidence of angioedema associated with angiotensin-converting enzyme inhibitors (ACE-I) has been estimated at 0.1%–2.2% of patients receiving treatment. Despite the potential severity of this disease state, standardized treatment is lacking. Traditional pharmacotherapy options include medications that target inflammatory mediators and the angiotensin pathway. However, because ACE-I-induced angioedema is caused by accumulation of bradykinin, these medications fail to target the underlying pathophysiology. Recently, novel therapies that target the kallikrein–bradykinin pathway have been studied. These include icatibant, ecallantide, C1 esterase inhibitors, and fresh-frozen plasma. Recent randomized controlled trials exhibit contradictory results with the use of icatibant. This is a focused review on traditional and novel treatment strategies for ACE-I-induced angioedema.