Question about Cushing's - Page 3Register Today!
- Jan 6, '06 by Keysnurse2008Quote from addnurseas i said...it is a "late sign" commonly associated with cushings.please re-read my post.it is a late sign commonly seen associated with cushings triad.is it one of the trio?no...no it is not. do you commonly see it as a late "ominous- as i said" sign in like for example (as i stated above )with grade 5 sah patients? yes...you do. and you are correct these patients are the "high risk/high mortality" group of patients that are often trying to herniate.we make interventions like the medically induced hypothermia and burst suppression to "attempt" to reverse partial herniation and maintain "any" cerebral function.cushings triad is really a trio of "early warning signs" for those that work in the neuroicu.when your pulse pressure widens it is a late ominous sign that interventions have to be made immediately or else you will proceed on to tentorial herniation and all brain stem functions will fade....brain death.a widening pulse pressure is something to really watch for closely when you are seeing cushings...it is a late ominous sign.when i think of cushings i think of our common everyday neurocardiogenic shock type patients that pretty much are seen in any grade 4-5 sah patients, large hemmorragic strokes etc etc. these are things we see pretty much every day...and are "aware" of.....but it is seen in the majority of patients that we deal with.widening pulse pressures = either extension of the bleed, massive cerebral edema or another event that is pressing that patient towards the grim reaper(tentorial/tonsillar herniation).hope i havent confused you...on what i was saying.its just alot of our patient population has all the elements of cushings or they probably wouldnt be in the neuro icu...so i watch for the latter ominous signs and of course treat anything we can treat early.cushings triad consists of hypertension, bradycardia, and hyperventilation in the presence of increased intracranial pressure. the widening pulse pressure that accompanies the hypertension is as a result of the increasing systolic pressure in an attempt to perfuse the brain, the only decrease in the diastolic that i have seen is after herniation and is not a component of cushings traid.
- Jan 7, '06 by ADDnurseNo you didn't confuse me, but thanks for asking. I am however glad that we seem to agree that a decrease in diastolic blood pressure is not a component of cushings triad, but occurs after someone has herniated, be it supra, intra, or subtentorial. I am however confused as to why any patient in a NSICU, with a grade 4-5 SAH, a large hemorrhagic stroke, or for that matter any trauma patient with a GCS <7(in the absence of drugs) would not have an ICP monitor, preferrably ventricular, or have their cerebral SVO2 monitored, both of which provide us with real time information that we can use to treat our neuroscience cases, instead of blindly waiting for them to herniate.
- Quote from addnurseaddnurse...you know some hcf's really agressively monitor icp,,,and when that icp crawls over 20 and stays there they see "this" as the time to agressively treat the patients with things like mannitol, 3% nacl to get them hypernatremic and dry that brain out, some utilize that "20" golden marker as the time to medically induce hypothermia , pentobarb comas etc etc etc.. i think alot of it just has to do with "if" that hcf is teaching or nonteaching.nonteaching hcf's tend to less agressively manage and monitor icp...and often times.....sad to say....its probably out of ethics considerations. meaning...these patients....that have really high icps like in the 40's ( have seen them as high as 142 icp) how much brain function are they truly going to have post swelling?(younger ones have better results)...but unless this is a teenager...the chances of this patient having anything but some basic brainstem functions is almost nill.so....they have agressively treated them....so that they can be vegatative and vent dependant for life.can you see what i am saying?...in a teaching hospital...those residents are there to learn.in a nonteaching hospital...they have stronger ethical standards(at times) and look beyond just getting that icp below 50...like what is the long term prognosis.beneficience-, ethics, its all highly political and controversial.no you didn't confuse me, but thanks for asking. i am however glad that we seem to agree that a decrease in diastolic blood pressure is not a component of cushings triad, but occurs after someone has herniated, be it supra, intra, or subtentorial. i am however confused as to why any patient in a nsicu, with a grade 4-5 sah, a large hemorrhagic stroke, or for that matter any trauma patient with a gcs <7(in the absence of drugs) would not have an icp monitor, preferrably ventricular, or have their cerebral svo2 monitored, both of which provide us with real time information that we can use to treat our neuroscience cases, instead of blindly waiting for them to herniate.
i am interested though in one thing you said...cerebral svo2 monitoring.tell me more....are you talking about a device that actually is placed like an evd....or with an evd that acts as like a spo2 monitor?if so...does it come with your evd....what are your parameters of normal and crisis values?
- Quote from addnursealso....widening pulse pressure doesnt mean someone has "already" herniated.....it usually means they are begining to...or have only partially herniated....and if treated aggressively...can often times be reversed.....but again.....unless this is a young teenager we are talking about you have only saved them for a vegatative-vent dependant life...which further and progressively traumatizes that family.so...its a highly ethical decision that needs to made jointly with the family and nsurgeon after....after....they have been told a truthful honest realistic cognitive rehab potential for the family to make the correct decision.no you didn't confuse me, but thanks for asking. i am however glad that we seem to agree that a decrease in diastolic blood pressure is not a component of cushings triad, but occurs after someone has herniated, be it supra, intra, or subtentorial. i am however confused as to why any patient in a nsicu, with a grade 4-5 sah, a large hemorrhagic stroke, or for that matter any trauma patient with a gcs <7(in the absence of drugs) would not have an icp monitor, preferrably ventricular, or have their cerebral svo2 monitored, both of which provide us with real time information that we can use to treat our neuroscience cases, instead of blindly waiting for them to herniate.
to be honest...most neuro icu nurses dont focus on cushings.they have to be pretty critical to meet admit criteria for a neuroicu....and that means that 99.999999% of them we see with the cushings triad.so,,...we know what weve got....we just look for the latter ominous signs like widening pulse pressure, anisocoria, overbreathing the vent to stop, icps to top and be maintained at over 20 as k e y signs to make needed interventions ...fast...depending on how aggressively that neurosurgeon and the "well informed family" want to treat the patient.hope this helps...
- Jan 7, '06 by ADDnurseA cerebral SVO2 monitor (we used pediatric SVO2 swan ganz caths) is placed in the external jugular vein at the jugular bulb and you simply use it to monitor the mixed venous oxygen saturation as it leaves the cerebral circulation thereby giving you a measurement that reflexes cerebral oxygen utilization. When the cerebral SVO2 dropped below 75%(it may have been 70, it's been a while since I left neuro) an intervention was needed to either increase O2 delivery, or decrease O2 consumption. Regarding CSF drainage we would only drain for sustained increases in ICP>25mmHg, except where the ICP waveform showed decreased compliance in which case we would diurese and drain.
Hope this helps, as I said it's been a while since I did neuroLast edit by ADDnurse on Jan 7, '06
- wow...neat use of a swan ganz cath.So you just utilize it like you would a swan only the placement site is different.Kinda neat idea....thanks for sharing!!!!
- Apr 23, '06 by jakabI was actually looking this up for a different reason on Google and stumbled across this forum - thought I would throw in my 2cents.
The increased pulse pressure (due to the lower diastolic blood pressure) could be a result of the decreased HR found in the Cushing response.
DBP is generally affected by two things, HR and total peripheral resistance.
As HR decreases there is more time for "run off" (transfer of blood from the arterial to the venous circulation) and therefore less arterial volume at the end of diastole.
The lower arterial volume gives you the lower DBP, which would indeed widen the pulse pressure.
- Apr 26, '06 by topkatI'm reading this out of Barker 2nd edition Neuroscience Nursing A Spectrum of Care
"Cushing's reflex is helpful in explaining the late signs of increased ICP. This response is seen with sudden increases in pressure that result from distortion of a pressure area in the medulla beneath the floor of the fourth ventricle. When the CSF pressure rises to equal arterial pressure, the arteries become compressed and blood supply to the brain is decreased. The vasomotor center becomes ischemic and triggers the arterial pressure to rise in compensation for low perfusion. A sympathetically mediated response causes the systolic blood pressure to increase, and there is a widening pulse pressure, slowing of the pulse, and irregular respirations. Patients presenting with Cushing's reflex have recovered after rapid treatment."
I also asked a Neurosurgeon who explained it this way.....as the systolic rises but the pulse drops, it's like there is more time for the diastolic pressure to fall since the pulse is slower..not a lot of pressure built up between beats., therefore the diastolic pressure is lower...does that make sense???
hope that helps....and it really was an excellent question... topkatLast edit by topkat on Apr 26, '06
- Jun 2, '06 by Ras TwakaThe Cushing Reaction is a combination of two events in response to cerebral ischemia:
1) Central chemoreceptors--in the brain--register an increase in PCO2 (increased pH) and stimulate vasoconstriction throughout the body to increase systolic pressure. Remember that the cerebral vessels do not have a great amount of muscle and therefore are not as succeptible to vasoconstriction.
2) The rise in peripheral BP (sensed by baroceptors in the carotid sinus and aortic arch) increases the rate of afferent (to the brain) firing of the nerves running to the brainstem (CN 9 and CN 10). This causes a reflex DECREASE in the firing of efferent SYMPATHETIC (and INCREASE in firing of efferent PARASYMPATHETIC) nerves to the heart resulting in BRADYCARDIA.
In short, Hypertension is the sympathetic response, and bradycardia is the parasympathetic response.
Hope this helps.