Microbiological pattern of arterial catheters in the intensive care unit

<p>Abstract</p> <p>Background</p> <p>Intravascular catheter related infection (CRI) is one of the most serious nosocomial infections. Diagnostic criteria include a positive culture from the catheter tip along with blood, yet in many patients with signs of infection, current culture techniques fail to identify pathogens on catheter segments. We hypothesised that a molecular examination of the bacterial community on short term arterial catheters (ACs) would improve our understanding of the variety of organisms that are present in this niche environment and would help develop new methods for the diagnosis of CRI.</p> <p>Results</p> <p>The whole bacterial community presenting on all ACs was evaluated by molecular methods, i.e., a strategy of whole community DNA extraction, PCR amplification followed by cloning and 16S rDNA sequence analysis. Ten ACs were removed from patients suspected of CRI and 430 clones from 5 "colonised" and 5 "uncolonised" (semi-quantitative method) AC libraries were selected for sequencing and subsequent analysis. A total of 79 operational taxonomic units (OTUs) were identified at the level of 97% similarity belonging to six bacterial divisions. An average of 20 OTUs were present in each AC, irrespective of colonisation status. Conventional culture failed to reveal the majority of these bacteria.</p> <p>Conclusions</p> <p>There was no significant difference in the bacterial diversity between the 'uncolonised' and 'colonised' ACs. This suggests that vascular devices cultured conventionally and reported as non infective may at times potentially be a significant source of sepsis in critically ill patients. Alternative methods may be required for the accurate diagnosis of CRI in critically ill patients.</p

Risk factors for peripheral intravenous catheter failure: a multivariate analysis of data from a randomized controlled trial

Objective.To assess the relative importance of independent risk factors for peripheral intravenous catheter (PIVC) failure.Methods.Secondary data analysis from a randomized controlled trial of PIVC dwell time. The Prentice, Williams, and Peterson statistical model was used to identify and compare risk factors for phlebitis, occlusion, and accidental removal.Setting.Three acute care hospitals in Queensland, Australia.Participants.The trial included 3,283 adult medical and surgical patients (5,907 catheters) with a PIVC with greater than 4 days of expected use.Results.Modifiable risk factors for occlusion included hand, antecubital fossa, or upper arm insertion compared with forearm (hazard ratio [HR], 1.47 [95% confidence interval (CI), 1.28--1.68], 1.27 [95% CI, 1.08--1.49], and 1.25 [95% CI, 1.04--1.50], respectively); and for phlebitis, larger diameter PIVC (HR, 1.48 [95% CI, 1.08--2.03]). PIVCs inserted by the operating and radiology suite staff had lower occlusion risk than ward insertions (HR, 0.80 [95% CI, 0.67--0.94]). Modifiable risks for accidental removal included hand or antecubital fossa insertion compared with forearm (HR, 2.45 [95% CI, 1.93--3.10] and 1.65 [95% CI, 1.23--2.22], respectively), clinical staff insertion compared with intravenous service (HR, 1.69 [95% CI, 1.30--2.20]); and smaller PIVC diameter (HR, 1.29 [95% CI, 1.02--1.61]). Female sex was a nonmodifiable factor associated with an increased risk of both phlebitis (HR, 1.64 [95% CI, 1.28--2.09]) and occlusion (HR, 1.44 [95% CI, 1.30--1.61]).Conclusions.PIVC survival is improved by preferential forearm insertion, selection of appropriate PIVC diameter, and insertion by intravenous teams and other specialists.Trial registration.The original randomized controlled trial on which this secondary analysis is based is registered with the Australian New Zealand Clinical Trials Registry (http://www.anzctr.org.au; ACTRN12608000445370)

Assessment of arterial stiffness, oxidative stress and inflammation in acute kidney injury

Background: It is well know that arterial stiffness, oxidative stress and inflammation are features of chronic kidney disease. The arterial changes have a multitude of potential interconnected causes including endothelial dysfunction, oxidative stress, inflammation, atherosclerosis and vascular calcification. There is evidence that arterial stiffness becomes progressively worse as CKD progresses. The contribution of the biochemical changes of uremic toxicity to arterial stiffness is less clear. The aim of this study is to elucidate the vascular changes in acute kidney injury. We hypothesise that arterial stiffness will be increased during acute kidney injury and this will return to normal after kidney function recovers

Metformin-induced lactic acidosis: a case series

<p>Abstract</p> <p>Introduction</p> <p>Unlike other agents used in the treatment of type 2 diabetes mellitus, metformin has been shown to reduce mortality in obese patients. It is therefore being increasingly used in higher doses. The major concern of many physicians is a possible risk of lactic acidosis. The reported frequency of metformin related lactic acidosis is 0.05 per 1000 patient-years; some authors advocate that this rate is equal in those patients not taking metformin.</p> <p>Case presentation</p> <p>We present two case reports of metformin-associated lactic acidosis. The first case is a 77 year old female with a past medical history of hypertension and type 2 diabetes mellitus who had recently been prescribed metformin (3 g/day), perindopril and acetylsalicylic acid. She was admitted to the emergency department two weeks later with abdominal pain and psychomotor agitation. Physical examination revealed only signs of poor perfusion. Laboratory evaluation revealed hyperkalemia, elevated creatinine and blood urea nitrogen and mild leukocytosis. Arterial blood gases showed severe lactic acidemia. She was admitted to the intensive care unit. Vasopressor and ventilatory support was initiated and continuous venovenous hemodiafiltration was instituted. Twenty-four hours later, full clinical recovery was observed, with return to a normal serum lactate level. The patient was discharged from the intensive care unit on the sixth day. The second patient is a 69 year old male with a past medical history of hypertension, type 2 diabetes mellitus and ischemic heart disease who was on metformin (4 g/day), glycazide, acetylsalicylic acid and isosorbide dinitrate. He was admitted to the emergency department in shock with extreme bradycardia. Initial evaluation revealed severe lactic acidosis and elevated creatinine and urea. The patient was admitted to the Intensive Care Unit and commenced on continuous venovenous hemodiafiltration in addition to other supportive measures. A progressive recovery was observed and he was discharged from the intensive care unit on the seventh day.</p> <p>Conclusion</p> <p>We present two case reports of severe lactic acidosis most probably associated with high doses of metformin in patients with no known contraindications for metformin prescription. In both patients no other condition was identified to cause such severe lactic acidosis. Although controversial, lactic acidosis should be considered in patients taking metformin.</p

Assessment of peripheral arterial catheters as a source of sepsis in the critically ill: A narrative review

Intravascular devices (IVDs) are essential in the management of critically ill patients; however, IVD-related sepsis remains a major complication. Arterial catheters (ACs) are one of the most manipulated IVDs in critically ill patients. When bloodstream infection (BSI) is suspected in a patient with an IVD in situ, clinicians have focused their attention on the central venous catheter (CVC) while largely ignoring the AC. Although it would be routine for the CVC to be cultured and replaced if necessary for suspected IVD or catheter-related sepsis, the AC may not be treated in the same manner. The reasons for this may in part relate to the patient groups studied. In lower acuity patients with short dwell times, AC sepsis rates are indeed low. In the higher acuity patient, earlier studies suggested that ACs had an infective potential at least equal to short term CVCs, a finding that has translated poorly into clinical practice. It has been estimated that there may be up to 48 000. BSIs per year arising from ACs in the USA alone, suggesting a significant clinical problem. Recent evidence now shows that the infective potential of the AC is comparable with that in short term CVCs regarding both colonisation (which precedes BSI) and BSI, consolidating earlier studies. In critically ill patients suspected of catheter-related bloodsteam infection it is suggested that both the AC and CVC must now be assessed together. © 2010 Published by Elsevier Ltd on behalf of The Hospital Infection Society

Pneumococcal meningitis masquerading as subarachnoid haemorrhage

A 43-year-old woman taking warfarin for past venous thrombosis presented with 4 days of flu-like symptoms and deterioration in level of consciousness. Computed tomography suggested subarachnoid haemorrhage, and magnetic resonance imaging showed widespread cerebral infarcts. However, these seemed out of proportion to the amount of haemorrhage, and lumbar puncture revealed meningitis caused by Streptococcus pneumoniae