Barbiturates in Critical Care

suzanne4, RN · Sep 20, 2005

Barbituate comas are still used all of the time. Remember that they are not used for their sedative properties, but to decrease any type of brain evoked potential. Propofol is wonderful for sedation in the Neuro ICU as you can turn it off, and then almost immediately do a neuro check and then turn it back up.

Hope that this helps........................

gwenith, BSN, RN · Sep 21, 2005

At one time we were commonly inducing head injuries into a "barbituate coma" as part of "neuro protection" however we discovered that the darn stuff took forever to wear off again making neuro assessment impossible. But as Susanne says - it is still used especially for intractable status epilepticus.

hope this helps..........

Elenaster · Sep 21, 2005

In my experience, barbituate comas are still used, but only as a last ditch effort for cerebral hypertension (not hydrocephalus) refractory to other treatments, such as mannitol in addition to what Gwenith stated.

Barbituate comas have some very negative side effects, such as pneumonia, paralytic ileus and severe skin breakdown Additionally its use delays brain death testing, as the drug must be out of the system entirely before testing can be initiated. Pentobarb is fat soluable and takes days to clear.

I have seen patients come out of barbituate comas and survive, but their quality of life is questionable (trached, pegged, in a nursing home). The majority of patients I've seen have died, either from complications or the progression of brain death.

gwenith, BSN, RN · Sep 22, 2005

Thanks Elanaster - I have not seen it except for a VERY intractable status epilepticus patient who was post surgery - we have used it occasionally for a very short term but nothing like we originally tried. Rotten stuff took two - three weeks to wear off - in the meantime you had a completely paralysed patient with all the negative outcomes that causes.

suzanne4, RN · Sep 22, 2005

It is still used in Pediatric ICUs, especially after severe traumatic brain injuries, when necessary.

mwbeah · Sep 25, 2005

Propofol is the hypnotic

agent of choice in patients with an acute neurologic

insult, as it is easily titratable and rapidly reversible

once discontinued. These properties permit predictable

sedation yet allow for periodic neurologic evaluation

of the patient.116,117 Propofol has additional

properties that may be beneficial in the head-injured

patient, including a decrease in cerebral metabolic

rate, potentiation of Gamma-aminobuturate A (GABAergic)

inhibition, and inhibition of methyl-D-aspartate

glutamate receptors and voltage-dependent calcium

channels.118 Propofol is also a potent antioxidant and

inhibitor of lipid peroxidation.119

Link: http://www.chestjournal.org/cgi/reprint/122/2/699

Elenaster · Sep 25, 2005

I agree that propofol is a far superior drug for providing sedation in ICU patients under most circumstances, however it should be noted that some patients experience a sustained drop in blood pressure that limits its use, particularly if they have increased ICP.

For those who are unfamiliar, it is exceedingly important to maintain cerebral perfusion pressure, usually greater than 60-70 mmHg, in a patient with high ICP. The formula is:

(MAP) - (ICP) = CPP

mwbeah · Sep 25, 2005

I agree that propofol is a far superior drug for providing sedation in ICU patients under most circumstances, however it should be noted that some patients experience a sustained drop in blood pressure that limits its use, particularly if they have increased ICP.
For those who are unfamiliar, it is exceedingly important to maintain cerebral perfusion pressure, usually greater than 60-70 mmHg, in a patient with high ICP. The formula is:
(MAP) - (ICP) = CPP

Are you implying...........?

Lets see, I work with propofol daily. When the BP drops, I believe that you turn the infusion down.....correct me if I am wrong..........

I am a Doctoral Neuroscience student.........I should know the formula..... (JK) :)

(One question, how can Right atrial pressure affect ICP?)

The CPP number which has been evidenced based is 70mmHg or above with injury:

Chan K H, Miller J D, Dearden N M, Andrews P J D & Midgley S. "The effects of changes in cerebral perfusion pressure upon middle cerebral artery blood flow velocity and jugular bulb venous oxygen saturation after severe brain trauma." J.Neurosurgery 1992; 77: 55- 61.

:)

hrtprncss · Sep 25, 2005

HI quick question, I know that sedation then let's say norcuron then barb coma, with concommitant use of mannitol and other things are being implemented. I just want to know how many people still use hyperventilation as a technique to decrease ICP, i know it's been basically supposedly phased out...But is anyone still hyperventilating a patient, post 24 hours, to well i don't mean to control ICP but used as a short term adjunct to temporary decrease it in emergent situations...Curious to know...hrtprncss

mwbeah · Sep 25, 2005

HI quick question, I know that sedation then let's say norcuron then barb coma, with concommitant use of mannitol and other things are being implemented. I just want to know how many people still use hyperventilation as a technique to decrease ICP, i know it's been basically supposedly phased out...But is anyone still hyperventilating a patient, post 24 hours, to well i don't mean to control ICP but used as a short term adjunct to temporary decrease it in emergent situations...Curious to know...hrtprncss

There is alot of literature (especially pediatric) which shows detrimental effects of prolonged hyperventilation (terrible ischemia). Short term (usually less then 6-8 hours) not too terrible but DO NOT abruptly stop, you have to slowly increase the CO2, an abrupt increase (as you know) is bad news.

Mike

mwbeah · Sep 25, 2005

there is alot of literature (especially pediatric) which shows detrimental effects of prolonged hyperventilation (terrible ischemia). short term (usually less then 6-8 hours) not too terrible but do not abruptly stop, you have to slowly increase the co2, an abrupt increase (as you know) is bad news.
mike

here is an abstract:

j neurosurg. 1991 nov;75(5):731-9.[color=#336699]related articles, [color=#336699]links

adverse effects of prolonged hyperventilation in patients with severe head injury: a randomized clinical trial.

muizelaar jp, marmarou a, ward jd, kontos ha, choi sc, becker dp, gruemer h, young hf.

division of neurological surgery, medical college of virginia, richmond.

there is still controversy over whether or not patients should be hyperventilated after traumatic brain injury, and a randomized trial has never been conducted. the theoretical advantages of hyperventilation are cerebral vasoconstriction for intracranial pressure (icp) control and reversal of brain and cerebrospinal fluid (csf) acidosis. possible disadvantages include cerebral vasoconstriction to such an extent that cerebral ischemia ensues, and only a short-lived effect on csf ph with a loss of hco3-buffer from csf. the latter disadvantage might be overcome by the addition of the buffer tromethamine (tham), which has shown some promise in experimental and clinical use. accordingly, a trial was performed with patients randomly assigned to receive normal ventilation (paco2 35 +/- 2 mm hg (mean +/- standard deviation): control group), hyperventilation (paco2 25 +/- 2 mm hg: hv group), or hyperventilation plus tham (paco2 25 +/- 2 mm hg: hv + tham group). stratification into subgroups of patients with motor scores of 1-3 and 4-5 took place. outcome was assessed according to the glasgow outcome scale at 3, 6, and 12 months. there were 41 patients in the control group, 36 in the hv group, and 36 in the hv + tham group. the mean glasgow coma scale score for each group was 5.7 +/- 1.7, 5.6 +/- 1.7, and 5.9 +/- 1.7, respectively; this score and other indicators of severity of injury were not significantly different. a 100% follow-up review was obtained. at 3 and 6 months after injury the number of patients with a favorable outcome (good or moderately disabled) was significantly (p less than 0.05) lower in the hyperventilated patients than in the control and hv + tham groups. this occurred only in patients with a motor score of 4-5. at 12 months posttrauma this difference was not significant (p = 0.13). biochemical data indicated that hyperventilation could not sustain alkalinization in the csf, although tham could. accordingly, cerebral blood flow (cbf) was lower in the hv + tham group than in the control and hv groups, but neither cbf nor arteriovenous difference of oxygen data indicated the occurrence of cerebral ischemia in any of the three groups. although mean icp could be kept well below 25 mm hg in all three groups, the course of icp was most stable in the hv + tham group. it is concluded that prophylactic hyperventilation is deleterious in head-injured patients with motor scores of 4-5.(abstract truncated at 400 words)