Faculty Bibliography

Ketamine, initially developed as an anesthetic, has shown versatility in medical applications, including pain management, treatment-resistant depression, and sedation in the intensive care unit (ICU). While generally well-tolerated, long-term use at high doses raises concerns about potential toxicities, particularly in the liver. We present a case of a 27-year-old female with a complex medical history who received ketamine infusion for ICU sedation and experienced a sudden rise in liver function tests (LFTs), indicating possible ketamine-induced liver injury (KILI). The patient's liver function normalized after ketamine discontinuation. KILI is infrequent with short-term ketamine use, but emerging case reports suggest it may be associated with chronic or intermittent exposure. The underlying mechanisms for KILI are not fully understood but may involve the accumulation of ketamine metabolites, causing direct toxic effects on the liver. As ketamine's use expands, especially in critical care settings, clinicians should be vigilant for the potential development of KILI. Further research is needed to better understand its risk factors and mechanisms, as early detection and management of KILI are crucial to ensuring patient safety and optimizing ketamine's therapeutic benefits.

PURPOSE/OBJECTIVE:PRIS is a potentially fatal syndrome characterized by various clinical symptoms and abnormalities. Experts suggest that propofol treatment duration ≥48 h or dose ≥83 μg/kg/min is associated with developing PRIS. We hypothesized PRIS might be underdiagnosed due to the overlap of PRIS clinical manifestations with critical illnesses. MATERIALS AND METHODS/METHODS:Multihospital, retrospective study of adult patients who received continuous propofol infusion ≥48 h or dose ≥60μg/kg/min for >24 h since admission were assessed for the development of PRIS. RESULTS:The incidence of PRIS was 2.9% with a PRIS-associated mortality rate of 36.8%. In PRIS patients, propofol was administered at a median dose of 36.4 μg/kg/min and over a median duration of 147.0 h. The development of PRIS was observed at a median of 125.0 h post-propofol initiation and a cumulative dose of 276.5 mg/kg. The development of metabolic acidosis (78.9%), cardiac dysfunction (52.6%), hypertriglyceridemia (100%), and rhabdomyolysis (26.3%) were observed in our PRIS patients. CONCLUSION/CONCLUSIONS:PRIS can often be overlooked and underdiagnosed. It is important to monitor for early signs of PRIS in patients who are on prolonged propofol infusion. Prompt recognition and interventions can minimize the dangers resulting from PRIS.

PURPOSE/OBJECTIVE:Measure the effect of inhaled pulmonary vasodilators on gas exchange in mechanically ventilated patients with COVID-19. METHODS:ratio, oxygenation Index (OI), and ventilatory ratio (VR) after initiation of inhaled pulmonary vasodilators. RESULTS:, OI and VR did not significantly change over a five day period starting the day prior to drug initiation in patients who received either iNO or iEPO assessed with a fixed effects model. CONCLUSION/CONCLUSIONS:Inhaled pulmonary vasodilators were not associated with significant improvement in gas exchange in mechanically ventilated patients with COVID-19.

Kawasaki disease is an acute, self-limited, febrile vasculitis typically seen in early childhood. Pulmonary involvement is uncommon and is not part of the conventional diagnostic criteria. We add to the literature a unique case of a 22year-old male with Kawasaki disease and pulmonary involvement. It illustrates the importance of recognizing unusual presentations of Kawasaki disease and highlights the possibility of pulmonary abnormalities on physical and imaging examination. Awareness of such presentations can help avoid delayed diagnosis, prevent the development of coronary aneurysms, and allow careful observation for imaging resolution.

Community-acquired pneumonia (CAP) encompasses a broad spectrum of disease severity and may require outpatient, inpatient, or intensive care management. Successful treatment hinges on expedient delivery of appropriate antibiotic therapy tailored to both the likely offending pathogens and the severity of disease. This review summarizes key principles in starting treatment and provides recommended empiric therapy regimens for each site of care. In addition, we discuss the antimicrobial and anti-inflammatory role macrolides play in CAP, as well as specific information for managing individual CAP pathogens such as community-acquired methicillin-resistant Staphylococcus aureus and drug-resistant Streptococcus pneumoniae. We also examine several novel antibiotics being developed for CAP and review the evidence guiding duration of therapy and current best practices for the transition of hospitalized patients from intravenous antibiotics to oral therapy.

PURPOSE OF REVIEW/OBJECTIVE:Community-acquired pneumonia (CAP) is a pervasive disease that is encountered in outpatient and inpatient settings. CAP is the leading cause of death from an infectious disease and accounts for significant worldwide morbidity and mortality. This update reviews current advances that can be used to promote improved outcomes in CAP. RECENT FINDINGS/RESULTS:Early recognition of CAP and its severe presentations, with appropriate site of care decisions, leads to reduced patient mortality. In addition to traditional prognostic tools, certain serum biomarkers can assist in defining disease severity and guide treatment and management strategies. The use of macrolides as part of combination antibiotic therapy has shown beneficial mortality effects across the CAP disease spectrum, especially for those with severe illness. When treating community-associated, methicillin-resistant Staphylococcus aureus pneumonia, use of an antitoxin antibiotic is likely to be valuable. Adjunctive therapy with corticosteroids may prevent delayed clinical resolution in selected patients with severe CAP. Recent data expand on the interaction of CAP with comorbid disease, particularly cardiovascular disease, and its impact on mortality in CAP patients. SUMMARY/CONCLUSIONS:Improved diagnostic tools, optimized treatment regimens, and enhanced understanding of CAP-induced perturbations in comorbid disease states hold promise to improve patient outcomes.