Conclusions: This study demonstrates a paradigm shift in the treatment of primary mycotic abdominal aortic aneurysms (MAAAs) in Sweden to the use of endovascular aneurysm repair (EVAR) as the preferred modality. EVAR was associated with improved short-term survival in comparison to open repair and without a higher incidence of serious infectious complications or reoperations.Summary: This retrospective study of a prospectively collected nationwide database spanned 10 years . All patients treated for a primary MAAAs were identified in the Swedish vascular registry (Swedvasc). The primary aim was assessment of survival after open repair (OR) or EVAR of a MAAA. Secondary end points were analysis of the rate of recurrent infections and reoperations as well as the time trends in surgical treatment. Propensity score-weighted correction for risk factors in the 2 groups was performed including the operative year to account for differences in treatment and outcome over time. One hundred and thirty-two patients were identified (0.6% of all AAA repairs) with mean age of 70. Rupture was the presenting symptom in 50 patients. Overall survival was 86% at 3 months, 79% at 1 year, and 59% at 5 years. The treatment modality shifted over this study, EVAR was not used prior to 2001 (n ¼ 14 repairs), jumped to 58% during 2001-2007 (n ¼ 43 repairs), and was used 60% of the time during 2008-2014 (n ¼ 75 repairs). Eight patients had multiple aortic aneurysms defined as a combination of infrarenal, paravisceral, and/or thoracic. The most common infectious agents were Streptococcus (22%), Staphlococcus (16%), and Salmonella (9%). Of the 62 patients treated with open repair, 50 were in situ reconstructions, 7 aortic resections and extra-anatomic bypasses, and 3 patch angioplasties. Two patients died

This study demonstrates a paradigm shift in treatment of MAAA in Sweden, with EVAR being the preferred treatment modality. EVAR was associated with improved short-term survival in comparison with OR, without higher associated incidence of serious infection-related complications or reoperations.

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The Swedish Reference Group for Antibiotics (SRGA) has carried out a risk-benefit analysis of aminoglycoside treatment based on clinical efficacy, antibacterial spectrum, and synergistic effect with beta-lactam antibiotics, endotoxin release, toxicity, and side effects. In addition, SRGA has considered optimal dosage schedules and advice on serum concentration monitoring, with respect to variability in volume of drug distribution and renal clearance. SRGA recommends that aminoglycoside therapy should be considered in the following situations: (1) progressive severe sepsis and septic shock, in combination with broad-spectrum beta-lactam antibiotics, (2) sepsis without shock, in combination with broad-spectrum beta-lactam antibiotics if the infection is suspected to be caused by multi-resistant Gram-negative pathogens, (3) pyelonephritis, in combination with a beta-lactam or quinolone until culture and susceptibility results are obtained, or as monotherapy if a serious allergy to beta-lactam or quinolone antibiotics exists, (4) serious infections caused by multi-resistant Gram-negative bacteria when other alternatives are lacking, and (5) endocarditis caused by difficult-to-treat pathogens when monotherapy with beta-lactam antibiotics is not sufficient. Amikacin is generally more active against extended-spectrum beta-lactamase (ESBL)-producing and quinolone-resistant Escherichia coli than other aminoglycosides, making it a better option in cases of suspected infection caused by multidrug-resistant Enterobacteriaceae. Based on their resistance data, local drug committees should decide on the choice of first-line aminoglycoside. Unfortunately, aminoglycoside use is rarely followed up with audiometry, and in Sweden we currently have no systematic surveillance of adverse events after aminoglycoside treatment. We recommend routine assessment of adverse effects, including hearing loss and impairment of renal function, if possible at the start and after treatment with aminoglycosides, and that these data should be included in hospital patient safety surveillance and national quality registries.

BackgroundRenal dysfunction is associated with increased morbidity and mortality in intensive care patients. In most cases the glomerular filtration rate (GFR) is estimated based on serum creatinine and the Modification of Diet in Renal Disease (MDRD) formula, but cystatin C-estimated GFR is being used increasingly. The aim of this study was to compare creatinine and MDRD and cystatin C-estimated GFR in intensive care patients.MethodsRetrospective observational study was performed, on patients treated within the general intensive care unit (ICU) during 2004–2006, in a Swedish university hospital.ResultsGFR markers are frequently ordered in the ICU; 92% of the patient test results had cystatin C-estimated GFR (eGFRcystatinC) ≤ 80 mL/min/1.73 m2, 75% had eGFR ≤ 50 mL/min/1.73 m2, and 30% had eGFR ≤ 20 mL/min/1.73 m2. In contrast, only 46% of the patients had reduced renal function assessed by plasma creatinine alone, and only 47% had eGFRMDRD ≤ 80 mL/min/1.73 m2. The mean difference between eGFRMDRD and eGFRcystatinC was 39 mL/min/1.73 m2 for eGFRcystatinC values ≤ 60 mL/min/1.73 m2.ConclusionsGFR is commonly assessed in the ICU. Cystatin C-estimated GFR yields markedly lower GFR results than plasma creatinine and eGFRMDRD. Many pharmaceuticals are eliminated by the kidney, and their dosage is adjusted for kidney function. Thus, the differences in GFR estimates by the methods used indicate that the GFR method used in the intensive care unit may influence the treatment.