G2 PILOT Posted November 28, 2011 Posted November 28, 2011 (edited) So I'm trying to wrap my brain around this (see what I did there?). For a patient with confirmed TBI, you would want to increase CPP while managing ICP. It seems like a gigantic blind-folded juggle with only capnography (and patient reaction) as your guidance. But I've tried breaking down the equation into what I can and cannot influence: ICP: Hyperventilation (low end of ETCO2; 30-35 mmHg); temporary relief, but the body will compensate and vasoconstriction leads to cerebral ischemia; Hypertonic solution -> reduces ICP through osmosis. MAP: Hypertonic solution -> elevates MAP; mannitol: diuretic effect, decreases cerebral edema. The delicate balance of ischemia versus herniation is confusing. Would it be better to err on the side of vasoconstriction (administration of vasopressor)? And am I missing anything from my theoretical treatment plan? Any thinking points would be welcome! Edit: For the sake of argument, let's say only a TBI and no other injuries. And apologies for double posting! My laptop went slow and I was overzealous on the submit key. Edited November 28, 2011 by G2 PILOT 1
BushyFromOz Posted November 28, 2011 Posted November 28, 2011 Without invasive ICP monitoring it not possible to really control or monitor you interventions. The effect of you vasopressor for instance could either be very good or very bad, but you will never know without a transducer in place. If you grab the algorithim you have and start playing with the digits (MAP and ICP) youll find that a B/P of 120 will maintain resonable CPP over the broadest range IF the ICP is not too high. Elevated systolic pressure is not necessarily good but it will maintain a reasonoable range of CPP. Moderate to severe hypotension, even in a patient with a ICP at the high end of normal is nearly always inadequate. So, mainating what you can. Keep the ETCo2 stable at 35mmHg ( I think the magic number escapes me) and treat hypotension. if they are coning there is nothing you can do except influence the time to difinitive care. Of course, i could have just made that crap up, but it sounds good 2
tniuqs Posted November 29, 2011 Posted November 29, 2011 Without invasive ICP monitoring it not possible to really control or monitor you interventions. The effect of you vasopressor for instance could either be very good or very bad, but you will never know without a transducer in place. Nothing further need be stated .. the use of tropes, mannitol are best left to ICU settings with mandatory ICP probe in situ. http://thejns.org/doi/pdf/10.3171/foc.2003.14.4.2 CONCLUSIONS Despite widespread recognition that systemic hypotension and intracranial hypertension are detrimental to the injured brain, the optimal CPP in patients with severe TBI and the relative importance of systemic blood pressure and ICP in contributing to optimal CPP remain debated.The normal pattern of CBF after brain injury is one of significant evolution over time. Furthermore, CBF may also vary markedly from patient to patient. For these reasons, consideration should be given to maintaining an optimal CPP in an individual patient at each specific moment in time, rather than having some arbitrary goal generalized in all patients. Monitoring of ICP together with continuous assessment of the adequacy of CBF by means of jugular venous oximetry and brain tissue PO2 monitoring are major components of CPP optimization. cheers
G2 PILOT Posted November 29, 2011 Author Posted November 29, 2011 Thank you for the link, tniuqs; I read it and found this nugget: For equivalent levels of CPP, cerebral perfusion is impaired more by reductions in blood pressure than by increases in ICP And I understand that I can't forsee what my interventions are doing in the case of TBI; My instructors have been pushing us to maintain first, second, third line defenses. So these are my take home points: Follow the curve; You can't get ahead of it. And in the event of falling BP, treat it. But not beforehand or else you have ischemia. Which makes vitals even more valuable since it can be tracked (please correct me if I'm wrong); Cushing's Triad of hypertension, irr. respirations, and bradycardia. 2
BushyFromOz Posted November 29, 2011 Posted November 29, 2011 Nothing further need be stated . Yeah i know, but i cant keep my trap shut!
tniuqs Posted November 29, 2011 Posted November 29, 2011 Yeah i know, but i cant keep my trap shut! It appears to be the Brisbane B strain is pandemic ? LOL
BushyFromOz Posted November 29, 2011 Posted November 29, 2011 It appears to be the Brisbane B strain is pandemic ? LOL for sure, im 2000 K's from brisbane!
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