Killol Patel

The Effect of Interdisciplinary Team Rounds on Urinary Catheter and Central Venous Catheter Days and Rates of Infection

Interdisciplinary team (IDT) rounds were initiated in the intensive care unit (ICU) in June 2010. All catheters were identified by location, duration, and indication. Catheters with no indication were removed. Data were collected retrospectively on catheter days and associated infections in a 20-month period before and after intervention with an aggregate of 19 207 ICU days before and 23 576 ICU days after institution of rounds. Results showed a statistically significant decrease in the number of indwelling urinary catheter (IUC) days (5304 vs 4541 days, P = .05) and catheter-associated urinary tract infection rates (4.71 vs 1.98 infections/1000 ICU days, P < .05). Central line days statistically increased after IDT rounds (3986 vs 4305 days, P < .05) but the catheter-related bloodstream infection rate trended down (3.5 vs 1.6 infections/1000 ICU days, P = .62). This analysis suggests that IDT rounds may have an impact on reducing the number of IUC days and associated infections.

1167: An Interesting Case of Propofol-induced Acute Hepatitis

Introduction: Case Report: Drug-induced liver injury is the leading cause of acute liver failure among patients referred for liver transplantation and the most common reason that drugs in development do not obtain approval by the Food and Drug Administration. Propofol is an anesthetic widely used in pediatric and adult populations, and propofol infusion syndrome has been well documented; however, there are very few published case reports implicating propofol infusion in acute liver injury. Five case reports were identified using PubMed: three occurred after gastrointestinal procedures, one after a varicose vein stripping procedure, and one after electroconvulsive shock therapy. We present the first documented case of acute hepatitis resulting from propofol use for induction and post-intubation sedation. We report a case of a 33 year-old hypertensive male who presented with a pontine hemorrhage. During his Intensive Care Unit (ICU) course, this patient was intubated and placed on a propofol infusion for sedation. He developed a transaminitis that resolved when the propofol infusion was stopped. We postulate that propofol was the underlying causative agent in this patients acute hepatitis. Case Description: A 33 year old hypertensive male without a prior history of liver disease presented with sudden collapse and was found to have a right pontine hemorrhage. He was intubated for airway protection in the Emergency Department (ED) without propofol. On day three of his ICU course, he failed a trial of extubation and was reintubated with propofol 140mg being used for induction but not for post-intubation sedation. On day four, he self-extubated and was again reintubated with propofol 150mg for induction. A propofol infusion was started for sedation at a rate of 5mcg/kg/min. On day six of his stay, the second day of his propofol infusion he was found to have a transaminitis with alanine transaminase (ALT) 656, aspartate aminotransferase (AST) 240 and alkaline phosphatase (ALP) 174. Right upper quadrant ultrasound was unremarkable with normal appearance of the liver in terms of size, configuration and echo content on the same day. The propofol infusion was stopped; the following day his repeat ALT was 482, AST 140 and ALP 133. The patients ALT, AST and ALP continued to trend down over the following six days to normal levels. Discussion: Inhibition of mitochondrial function has been proposed as a potential mechanism by which propofol may cause accumulation of free fatty acids within hepatocytes, hepatic steatosis and acute liver injury. Genetic studies have identified differences in propofol metabolism and have proposed this as a factor in rare instances of propofol-induced hepatic injury. One case report described the use of drug lymphocyte stimulation testing as a potential tool in identifying patients with propofol induced liver injury. The growing number of case reports documenting hepatic injury after propofol administration may indicate a significant unrecognized clinical burden of disease. A simple screening tool has recently been proposed for propofol infusion syndrome. We submit that a similar screening tool for propofol induced hepatic injury would be valuable to clinicians. Further research is required to delineate the incidence of this syndrome in clinical practice and to develop tools to aid clinicians in the identification of susceptible individuals.