ender

Hey, I'm a new nurse. today, i was positioning a resident alongside another nurse when she put the catheter tubing under the resident's leg and a pillow under his foot. i was trained to place catheter tubing over resident leg, securing to either thigh or abdomen depending on gender and having catheter bag on the side of bed resident is facing...rationale being that tubing won't get kinked/compressed, prevents skin breakdown, and less likely to get pulled. the other nurse stated that "urine doesnt go uphill." as for positioning of feet, resident on a roho mattress. I'd place under legs to off load pressure from hells; however, other nurse stating there is peripheral vascular risk, though res has no dx of PVD. having said that, a cushion under heels doesn't seem to protect heels, esp if a roho mattress is already in use. It would seem more reasonable to avoid use of said pillow in the case of PVD. Is there any right answer?

i understand that. in the case of insulin r/t hypoglycemia (say giving insulin to a pt with BS 6 mmol/L and pt doesn't eat), would the insulin convert glucose-to-glycogen faster than glucagon converts glycogen-to-glucose, causing hypoglycemia. also, considering the fact that no sugars are being absorbed from missing said meal, relying on glucagon/glycogen storage from the liver will eventually deplete. brain needs sugar transport from the bloodstream to receive glucose, so if glucose levels decrease in the blood, then eventually neurological deficits (loc, motor skills, etc) will develop from lack thereof glucose...brain cannot use fats and protein. Thanks, I'm trying to work this out in my head.

I need clarification re: hypo/hyperglycemia. I understand it for what it is, just need clarification as to how it affects the body. For instance, I realize hyperglycemia is the resultant of high blood sugars and lack of insulin. furthermore, insulin converts glucose into glycogen for storage, so that it's not so high in the bloodstream. So, my question: is the problem in hyperglycemia r/t the high levels of glucose causing toxicity or the body needs insulin in order for cells to use said glucose, not just to convert into storage? the latter makes sense, since the body begins to breakdown ketones for cellular usage. as for hypoglycemia, my understanding is that there is not enough sugars/glucose for cells to use, creating hypoglycemic symptoms, esp neurologically wherein the brain cannot use fats and/or proteins for breakdown to get energy. having said that, the body can convert the glycogen back to glucose for uptake. if its insulin r/t, is it because the insulin is simply converting any glucose back to glycogen? making there be no glucose available for cellular metabolism? I feel like I have the fundamental understanding, but want to grasp the "big picture" of a very real disease that is making so many lives difficult. Thanks.

hey, so i went to visit my grandfather who in July was in a coma for 2 weeks, following a massive MI, only to take notice that his sugars have been as high as 30mmol at dinner and as low as 17mmol in the morning (fasting) for the past month. my knowledge of diabetes is fair. i deal with it at work on daily basis; however, sugars are not this high. if they do become out of control, then i'm always a telephone call away from receiving an order to lower said sugars. so, as i understand it, if theres not enough insulin, then cells cannot use sugars for metabolism; thus, ischemia begins to occur (pvd, retinopathy, neuropathy, eventually nephropathy and heart disease and stroke). lipids and proteins are broken down for uptake by cells that are deprived of glucose, leading to surplus of ketones (metabolites of proteins and fats), causing ketoacidosis (metabolic acidosis =decrease in body ph). my grandfather has 2 scheduled dosages of humulin 30/70 36 units at breakfast and dinner. at first glance, i asked what he had been consuming, though no exact meals stated. i then asked if they had contacted their family doc re: chronically high sugars. they stated they had not talked to their doc since discharge. so, i told them to make an appointment tomorrow, as well as logging his meals for the next 2 weeks and taking his sugars at noon in addition to BGMs at 0800 and 1700. i told her to be conscious of his intake of high sugar meals (reading the nutritional facts), and encouraged consumption of plenty of water. i'm going to follow up at the end of this week with them (as i'm working a lot this week). any ideas as to what else i could do? or any knowledge i'm missing?

thanks everyone!!! this confirms exactly what i was thinking. i work in a nursing home with nurses having worked 20 years in said nursing home. lets just say- they're set in their ways. iv isn't possible in such setting. i enjoy the idea of using opposite sites (left and right vastus lateralis), though many of the res don't take too kind to it, so that's why i was thinking deltoid and vastus.

hello, i'm a new grad, so there's been a lot of things i'm having to deal with. an issue came about the other day at my place of work re: administration of rocephin IM injection. dr ordered 1g rocephin which we are to reconstitute with 3.3ml of 1% lidocaine in totaling a volume of 4ml to give to resident, producing a concentration of 0.25g/ml. as i have never had to reconstitute before, i turned to the rn, as i know an im site is unable to tolerate more than 3ml. the rn told me to give the res only 3ml of the reconstituted solution. however, in my mind, then the res would not be receiving the ordered dose as prescribed by doctor (having only received 750mg of said rocephin). i don't know if the rn is just not as adamant about giving the prescribed dose as me or i'm missing something. in my opinion, the dose would have to be split up with 3ml given to one im site (vastus lateralis, ventroglutel) and the remaining 1ml given to another im site (deltoid). any ideas?