[IL(E)14] An update of the subtleties of infection management in the ICU
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Professor Jeffrey Lipman received his medical degree (MBBCh) from the University of Witwatersrand, South Africa and has specialist qualifications in anaesthesia (DA, FFA) and intensive care (FFA Crit Care, FCICM).
Professor Lipman is Professor and Head of Anaesthesiology and Critical Care, University of Queensland and also is the Executive Director of the Burns, Trauma, Critical Care Research Centre at this University. He has Professorial attachments at QUT, University of New South Wales, Chinese University of Hong Kong and his Alma Mater, University of Witwatersrand.
He is a career Intensivist, having worked full-time in Intensive Care Units since 1979. His research interests include all aspects of infection management in intensive care. He has a special interest in the pharmacokinetics of antibiotics, an area in which he completed his MD through the Chinese University of Hong Kong where he still holds an Adjunct Professorial position.
He has published over 30 book chapters and over 500 peer-reviewed articles including in high impact journals like NEJM, JAMA and Lancet Infectious Diseases.
He has been an invited speaker to over 100 Congresses Nationally and Internationally, being a Keynote speaker in many countries around the world.
Sepsis is one of the leading causes of mortality and morbidity in the patients admitted to intensive care units (ICU). Despite evolving concepts and advances in management, the mortality associated with sepsis remains unexpectedly high. Early and appropriate antibiotic therapy has been the mainstay of treatment. There are however many unspoken subtleties in managing critically ill patients.
Firstly antibiotics (particularly broad spectrum) cause “collateral damage”, killing “good” commensal bacteria allowing resistant bowel organisms to grow. Currently the various syndromes we label as sepsis are often vague and poorly defined, predisposing to over use of antibiotics in inflammatory syndromes the causation of which may not be “infective”. New diagnostic genomic testing of host (patient) white cell mRNA may help differentiate the infective syndromes from other similar inflammatory conditions (1). A “watch and wait” philosophy for antibiotic initiation in the ICU in patients that are not acutely deteriorating has in fact been show to improve outcomes over a period of time (2). The importance of source control in managing patients with sepsis cannot be overemphasised (3). Finally, the longer a course of antibiotics is administered, the more the development of resistant bacterial overgrowth within the patients’ bowel, so shorter courses of antibiotics should be embarked upon where appropriate (4,5).
REFERENCES
1. PLoS Med. 2015 Dec 8;12(12):e1001916. doi: 10.1371/journal.pmed.1001916
2. Lancet Infectious Diseases 2012;12:774-80
3. BMC Infect Dis. 2014 Nov 28;14:193. doi: 10.1186/1471-2334-14-193
4. Crit Care Resusc. 2009 Dec;11(4):276-81
5.https://accpjournals.onlinelibrary.wiley.com/doi/abs/10.1002/phar.2201#.XBqsnRIK1FE.twitter
Firstly antibiotics (particularly broad spectrum) cause “collateral damage”, killing “good” commensal bacteria allowing resistant bowel organisms to grow. Currently the various syndromes we label as sepsis are often vague and poorly defined, predisposing to over use of antibiotics in inflammatory syndromes the causation of which may not be “infective”. New diagnostic genomic testing of host (patient) white cell mRNA may help differentiate the infective syndromes from other similar inflammatory conditions (1). A “watch and wait” philosophy for antibiotic initiation in the ICU in patients that are not acutely deteriorating has in fact been show to improve outcomes over a period of time (2). The importance of source control in managing patients with sepsis cannot be overemphasised (3). Finally, the longer a course of antibiotics is administered, the more the development of resistant bacterial overgrowth within the patients’ bowel, so shorter courses of antibiotics should be embarked upon where appropriate (4,5).
REFERENCES
1. PLoS Med. 2015 Dec 8;12(12):e1001916. doi: 10.1371/journal.pmed.1001916
2. Lancet Infectious Diseases 2012;12:774-80
3. BMC Infect Dis. 2014 Nov 28;14:193. doi: 10.1186/1471-2334-14-193
4. Crit Care Resusc. 2009 Dec;11(4):276-81
5.https://accpjournals.onlinelibrary.wiley.com/doi/abs/10.1002/phar.2201#.XBqsnRIK1FE.twitter