Ultrasound-guided peripheral intravenous access in chronic kidney disease patients.

OBJECTIVE: Ultrasound-guided peripheral intravenous (USPIV) catheters are being placed in emergency department (ED) patients with increasing frequency. USPIV catheters have been shown to improve the success rates of cannulation. It is unknown what the long-term effect of USPIV placement will be on fistula creation in chronic kidney disease (CKD) patients considering these ultrasound-guided peripheral lines often target the same deeper vessels used for fistulas. This study aimed to survey whether emergency medicine programs place restrictions on USPIV placement in patients with CKD stages 3-5. METHODS: This was a survey study encompassing all 110 emergency ultrasound fellowship directors in the United States at the time the survey was conducted. Data was collected on an anonymous and voluntary basis. The primary outcome was the number of programs with restrictions on USPIV placement in patients with CKD stage 3 or greater. RESULTS: Of the 56 programs that responded, 21% reported having policies limiting which patients were appropriate for USPIV. Despite this, only one program reported placing restrictions on USPIV in CKD stage 3 or greater (p < 0.0001). CONCLUSIONS: Emergency departments do not have or follow restrictions placed on USPIV placement in patients with CKD stage 3 or greater. The use of these veins in the ED may result in thrombosis as well as inflammation and permanent scarring which could negatively impact the ability to utilize those vessels for fistula creation. Future studies are needed to further characterize the impact of USPIV on fistula creation.

Metabolic dysfunction in obstructive sleep apnea: A critical examination of underlying mechanisms.

It has recently become clear that obstructive sleep apnea (OSA) is an independent risk factor for the development of metabolic syndrome, a disorder of defective energy storage and use. Several mechanisms have been proposed to explain this finding, drawing upon the characteristics that define OSA. In particular, intermittent hypoxia, sleep fragmentation, elevated sympathetic tone, and oxidative stress - all consequences of OSA - have been implicated in the progression of poor metabolic outcomes in OSA. In this review we examine the evidence to support each of these disease manifestations of OSA as a unique risk for metabolic dysfunction. Tissue hypoxia and sleep fragmentation are each directly connected to insulin resistance and hypertension, and each of these also may increase sympathetic tone, resulting in defective glucose homeostasis, excessive lipolysis, and elevated blood pressure. Oxidative stress further worsens insulin resistance and in turn, metabolic dysfunction also increases oxidative stress. However, despite many studies linking each of these individual components of OSA to the development of metabolic syndrome, there are very few reports that actually provide a coherent narrative about the mechanism underlying metabolic dysfunction in OSA.