NeuroICURN

Why would you email? That just sounds a little cowardly. Why not tell her face to face? If you absolutely NEVER see your manager, then call and leave a voicemail.

BTW....why wasn't this addressed by your preceptor? I know I read all the charting done by any orientee with me...then we sit and review what's right and wrong and she fixes what's wrong (thank goodness we have electronic charting). In the case of somewhere with paper charting....you probably should have done what I did in nursing school, which was write out my note on another piece of paper and have it reviewed before writing it. It would have taken a little longer, yes, but it would have saved a lot of headache now....agree?

Just because they can get in trouble for it, doesn't mean it shouldn't be charted!! If you were actually told that...I would get the heck out of there!! I agree that charting in a LTC facility and a hospital are very different, but that being said.....I chart so that if I get called into court 7 years from now, I can look back at my charting and tell you exactly what was going on with that patient. And as my instructors once drilled into my head........"If you don't chart it, it didn't happen".

I actually recommend telling your employer right away. Depending on the unit will depend on they handle it. On our unit, we don't make any of our pregnant nurses take ANY kind of isolation assignment. They could, but just as a courtesy, we don't make them do it. Also, we try to avoid giving pregnant women any combative or grossly overweight patients. Now, that being said...let me get a gripe out too. Pregnancy is NOT a disability. I hate when women use the excuse that they're pregnant to sit on their butt and only do the absolute bare minimum! There's usually no reason that you can't continue to do almost everything that you did before you were pregnant. Therefore, if you were doing a physical job before and you have a normal pregnancy, then there's no reason that you shouldn't be able to continue to do that job. I've also worked with many nurses who worked up until they delivered, with no problems. Even work with one now who went off her birth control to have a hip replacement and got pregnant before the surgery and now she's back to work; pregnany and really bad hip....now that's a strong girl! Now before anyone goes off and starts flaming...yes, I've been pregnant and yes, I continued everything that I did before...even competitive dancing early in the pregnancy and continuing to train till I delivered. Ok...just my two cents....

I'm with Gwenith on this one..... On neuro patients, we rarely ever go above 5, but have seen as high as 10...then other vent. methods start being used....i.e. pressure control ventilation or whatever is appropriate. Now with these patients, our intensivists handle their vents, etc. On trauma patients, I've seen as high as 15, but that's about it. With those, the trauma service tends to handle all their own stuff.....medical management, etc....but I do see a little change coming with that. They've been using the intensivists more now too. Our intensivists are also pulmonologists (dual specialties), so our vent management is some of the best you'll ever see....those guys are AMAZING!!! IMHO, we have some of the BEST critical care medical management you'll ever see!!

Did they try 3% NaCl? A bolus (typically 2-4 mL/kg) and then start a gtt??

omg...I can't believe I forgot to mention that! Thanks! Also, thanks to whoever mentioned about the PFO...I've seen a LOT of people with PFOs, but never knew there was a link with migraines. I'll have to look more into that. See....you learn something everyday.

Not to get too nosy here....but have you had a CT (to check for any bleeding or tumor), and/or a CTA (CT Angio) done?? If not, and your symptoms are this severe, you NEED to have that checked. Many people don't often have a warning to the fact that they have a brain aneurysm....but those that do, it's often migraine headaches. Also, the migraine headaches beforehand can be a warning that it's going to rupture. If you do end up having one and it's giving you these kind of symptoms, you need to see a neurosurgeon ASAP.....because when brain aneurysms do rupture, more than 50% never live to see a hospital and trust me when I say, the sequalae after a rupture is brutal!!

In our ICU, we are also responsible for all of the patient care (bathing, linen changes, etc.), but when we have an NA on, they will help you with that stuff. Our NAs also do our blood glucose monitorings, stock our bedsides and help us with our roadtrips. Our linens are stocked in a room, so other than an extra pad or pillowcase, we don't keep too much linen at the bedside. We do all of our own IV starts and blood draws, but there are techs that come around for EKGs and RT does our ABGs. As for our procedure trays, most of those come from central and it's the NAs job to make sure it's there. As someone previously explained, many ICU patient's have so many tubes and wires hanging out of them, that it requires a little finesse when doing even basic nursing care. A little interesting thing that we do with our crash carts is that ours are kept on the unit (we have 3) and have a little plastic lock on them (all you have to do is give it a little pull and it comes right off). Then, after a code, the US calls and central brings up a whole new, stocked and locked cart and they take the used one away. It's kinda nice because as long as you see the lock still on there, you know it's stocked and ready to go.

Personally, I would recommend an ICU. You'll typically get more experience with drips, lines, etc. Not that you don't get that in the ER, but you see it more in ICU because you don't have to deal with all the other stuff (i.e. flu pts, people just drug seeking, etc.) in the ICU. JMO

Honestly....sounds like the patient probably freaked out a little and it was probably more anxiety (and drama), than anything else. I've done more halo braces at the bedside than I remotely care to discuss. We do ours with the neurosurgeon, the orthotics guy and us (we're conscious sedation certified). I've never had this type of reaction from a patient. Frankly, I'm a fan of fentanyl and a little versed....along with the lido, of course. However, there's no need for deeper sedation. Most remember it...but I wouldn't call it a recipe for PTSD. And whoever recommended ketamine....ugh. Most patient's report some discomfort (it's darn near impossible to get rid of all the pain of the procedure), but overall, it's a well tolerated procedure. Some patients require the hand holding and distraction/relaxation techniques, but hey, that's what we're here for anyway, right? Just my 2 cents.

Congratulations to you too Roxan!!! That test was brutal, wasn't it?? I really had a hard time with the floor and rehab stuff since all I've ever done was Neuro ICU! I'll tell you what, that's a certification that I'll NEVER let slide and expire!! (I know someone who did and had to retake it, isn't that nuts?!?!) Take care!

:monkeydance: I'm so excited, that I had to share this with all of you....I passed the CNRN!!! Talk about being shocked...I couldn't believe it!! :monkeydance:

Ok, I got this from the article: Administering Hypertonic Saline to Patients With Severe TBI - on Medscape. If I could figure out how to insert a link to the article, I would. But, if you go to http://www.medscape.com and type in "hypertonic saline" in the search area, it will bring up the full article. Osmotic Effect HTS exerts an osmotic effect. It draws fluid out of edematous cerebral tissues because it has a higher concentration of sodium and a lower concentration of water than blood. When HTS is administered intravenously, plasma osmolarity increases. The higher sodium concentration causes blood to be hypertonic compared to cerebral tissue, which has a lower sodium concentration. These concentration differences set up an osmotic gradient that promotes the flow of excess water from cerebral tissue to the blood via osmosis. Osmosis occurs because water moves passively along the concentration gradient. Water moves from areas of lower concentration to areas of higher concentration (Feig & McCurdy, 1977). This osmotic effect can be used to combat cerebral edema. By reducing the water content of the injured brain, HTS can reduce mass effect. HTS can also control ICP, leading to a decrease in secondary brain injury (Qureshi & Suarez, 2000; Qureshi et al., 1998; Qureshi, Suarez, Castro, & Bhardwaj, 1999). Hemodynamic Effect The hemodynamic effect of HTS occurs because it is an effective plasma volume expander. Volume expansion improves blood pressure and cerebral perfusion pressure. Improved perfusion yields better oxygenation to areas of the brain that are at risk for secondary damage (Doyle et al., 2001; Kramer, 2003). Vasoregulatory Effect The use of HTS may also have beneficial effects on cerebrovascular regulation in the brain's microcirculation. Decreasing edema in the vascular endothelium of injured tissues lowers vascular resistance, allowing more blood to flow through the vessels. Thus, HTS modulates the hypoperfusion often seen in secondary brain injury. The effective increase in microvessel diameter can also help the injured brain combat hyperemia by allowing blood to flow out of the region (Doyle et al., 2001; Kramer, 2003; Pascual, Khwaja, Chaudhury, & Christou, 2003). Immunomodulatory Effects HTS can play a role in enhancing the immune modulation of brain cells. Head trauma can activate the inflammatory cascade, causing leukocytes to migrate and adhere to injured neurons. This inflammatory process can ultimately cause the injured cells to die. HTS, by a mechanism that is not yet fully established, can prevent leukocytes from becoming activated and adhering to brain cells, minimizing secondary pathologic events (Hartl et al., 1997). Neurochemical Effects HTS has neurochemical properties. After TBI, neuronal membranes may become destabilized, and the neurochemical environment can be disrupted. As a result, detrimental excitatory amino acids accumulate, leading to eventual cell death. HTS may modulate this process by normalizing neuronal cell membranes, by restoring normal electrolyte and neurotransmitter levels in brain cells, and by restoring normal cell volumes. Thus, HTS can limit secondary injury from neurochemical changes (Suarez, 2004). Hypernatremic Effect HTS has an important role in countering hyponatremia in the brain. Low serum sodium levels following TBI can lead to extracellular volume depletion, cerebral ischemia, and cerebral edema. These can all result in dangerous increases in ICP. HTS can help avoid the negative effects of hyponatremia by increasing serum sodium levels in the acute phase of head trauma care (Johnson & Criddle, 2004; Suarez, 2004). Ok, well hope this gives you the info. you need! Take care, NeuroICURN

Hey guys! To the poster that asked if the patient was on any kind of anticonvulsant - It is not uncommon to have a patient who is multiple anticonvulsant drugs and the patient remains in status (continues to have seizures). Now, that being said...It is not uncommon at all to use Propofol for seizure control. When someone comes in in status and the traditional drugs (i.e. Dilantin, phenobarbitol, etc.)....they very often end up intubated and we sedate them on Propofol. However, unlike other neuro patients on propofol, we don't do frequent wake-ups....that would be counterintuitive! So, what do we do when seizures are controlled by the drug but their BP drops....of course we try the fluid boluses and if that doesn't work, they get a pressor, but we usually start with Neo (phenylephrine). So, what to do when propofol doesn't even work? Well, we have other options. I've seen cases that were so bad that we've resorted to Ketamine gtts and Pentobarb comas. Also, I think it goes without saying that most of these patients get continuous EEG monitoring. We even had a guy one time that had seizures for 2.5 months!!! Believe it or not, he actually came out normal!!!