Often times, when "med math" is discussed, someone will pipe in with something along the lines of "well, the pharmacy actually does that... we just verify it," or "we use 'smart pumps.'"
Here's a real-world example from yesterday...
Ambulance delivers a patient who'd taken a header from the third floor balcony... obvious severe head trauma...
The patient gets intubated and needs to go to the scanner STAT. He's just starting to brady down a bit, "Bolus him 75 grams of mannitol and get him to the scanner now."
Our pyxis holds mannitol available as 20% mannitol in 250 mL of D5W.
1) The guy was GCS 6 on arrival and intubated immediately. ED and Trauma docs didn't order a sedation drip... despite the fact that paralytic and anesthesia were short-acting... why not? (hint... any other assessments needed?)
2) What other meds were ordered in quick succession after returning from CT?
3) What other MD intervention did we need to get set up for?
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Oh gosh...well, critical care is next semester for me, but I will take a stab at it!
So, I would think that ICP would be monitored as well as spinal issues from the fall. I would think the biggest issues with a head trauma like that would be autonomic issues from the ICP and injury. I would think respiratory and temperature control are biggies, as well as watching for CSF leakage. I would also think BP control would be a big issue...blood loss (?) and diuretics to control the ICP could lead to big drop, but I did remember from some of the neuro we've covered that Cushing's triad was a late ICP sign. The pt could have dysrhythmias r/t damage to the brain.
I would think an antipyretic for temp control, some type of fluid replacement, and something for pain management. I would think that blood glucose would need to be monitored, as well as all things pituitary-related (SIADH, etc) because I would imagine any massive injury like that could mess with hypothalamus and/or pituitary. Possibly an anti-seizure med as well?
There's my spitballing LOL. I am sure I'll be thinking back on this post when we cover these kinds of injuries in critical care I'll be watching for the follow-up to this!
edited to add...I thought of this but forgot to ask, at what GCS level do you discuss and make provisions for organ procurement, if it applies? (I know you said he was at a 6, but I can't imagine they leave all of that undealt with or at least discussed with a severe head injury and a low GCS score) I was wondering about that...
Specializes in Critical Care, ED, Cath lab, CTPAC,Trauma.
I'm going to refrain from answering I like where this is going....organ procurment conversation usually do not occur "immediately" although they are a part of admission paper work in most states.
An arrival GCS of 3 is pretty ominous.
You still need to think about why no sedation. The patient has a GCS of 6 and you gave Mannitol for cerebral edema and elevated ICP what would you be looking for on the patient to see if the Mannitol is effective.
I'm going to refrain from answering I like where this is going....organ procurment conversation usually do not occur "immediately" although they are a part of admission paper work in most states.
An arrival GCS of 3 is pretty ominous.
You still need to think about why no sedation. The patient has a GCS of 6 and you gave Mannitol for cerebral edema and elevated ICP what would you be looking for on the patient to see if the Mannitol is effective.
Sorry if I am hogging this thread...I love trying to think these thing through!
I am going to say that giving the mannitol is to help decrease edema to help increase perfusion, and increased perfusion should lead to increased LOC and a higher GCS score. As far as the sedation, wouldn't sedation cause hypotension? And wouldn't that be counter-productive? And if the patient is sedated I wouldn't think you could assess changes such as verbalization?
I think tomorrow I will do some reading on brain injuries...my curiosity has been piqued
Specializes in Critical Care, ED, Cath lab, CTPAC,Trauma.
Sorry if I am hogging this thread...I love trying to think these thing through!
I am going to say that giving the mannitol is to help decrease edema to help increase perfusion, and increased perfusion should lead to increased LOC and a higher GCS score. As far as the sedation, wouldn't sedation cause hypotension? And wouldn't that be counter-productive? And if the patient is sedated I wouldn't think you could assess changes such as verbalization?
I think tomorrow I will do some reading on brain injuries...my curiosity has been piqued
We have a winner! The patient is intubated so they can't talk.
We have a winner! The patient is intubated so they can't talk.
I am going to take a gander at this section in my critical care book today, so maybe I should refrain from asking questions until I read a bit...but I'll throw the questions out there and maybe after I read I can answer them or perhaps not LOL. So I won't take the win because I still don't fully understand this. So in this case if the patient is intubated (and I have yet to care for or even see an intubated patient, so please bear with me) they won't sedate because he can't talk? As a member of the care team is the GCS score what you're using as a gauge for progress/decline? My line of thinking in my answer was that GCS is being used as that gauge, so you're looking at three specific parameters (verbalization being one of them) and if the patient is sedated you can't assess a verbal response or pain response...so even if the patient can't talk because he's intubated, is it that you're looking more at the other specifics of GCS? And wouldn't a patient who's intubated fight the tubing if their LOC increased? (Like I said, I've never seen an intubated patient, but I remember every darn episode of any medical show in which a patient is intubated and becomes conscious they freak out at the tubing...Ha! How's that for reasoning behind an answer LOL!)
So, BP does not play a part in the reasoning behind no sedation? I keep coming back to looking for decrease of cerebral edema and increase in perfusion so I was thinking any BP changes would counteract the effects of the mannitol?
Anyhoo, just thinking out loud I'll do some reading on this today and see if I can better understand the whole process.
Edited to add: Holy cow, sorry for the ginormous post!!!
Specializes in Critical Care, ED, Cath lab, CTPAC,Trauma.
I am going to take a gander at this section in my critical care book today, so maybe I should refrain from asking questions until I read a bit...but I'll throw the questions out there and maybe after I read I can answer them or perhaps not LOL. So I won't take the win because I still don't fully understand this. So in this case if the patient is intubated (and I have yet to care for or even see an intubated patient, so please bear with me) they won't sedate because he can't talk? As a member of the care team is the GCS score what you're using as a gauge for progress/decline? My line of thinking in my answer was that GCS is being used as that gauge, so you're looking at three specific parameters (verbalization being one of them) and if the patient is sedated you can't assess a verbal response or pain response...so even if the patient can't talk because he's intubated, is it that you're looking more at the other specifics of GCS? And wouldn't a patient who's intubated fight the tubing if their LOC increased? (Like I said, I've never seen an intubated patient, but I remember every darn episode of any medical show in which a patient is intubated and becomes conscious they freak out at the tubing...Ha! How's that for reasoning behind an answer LOL!)
So, BP does not play a part in the reasoning behind no sedation? I keep coming back to looking for decrease of cerebral edema and increase in perfusion so I was thinking any BP changes would counteract the effects of the mannitol?
Anyhoo, just thinking out loud I'll do some reading on this today and see if I can better understand the whole process.
Edited to add: Holy cow, sorry for the ginormous post!!!
You are not way off base in your thinking.
The patient came in...no sedation....with a GCS of 6 indicating a severe head injury. With a decreased LOC the patient would have trouble managing their airway and will probably have decreased respiration which will increase the CO2 in the blood leading to further decreased LOC and brain swelling.
Just prior to transport to another department the are showing signs of further increased ICP...you are partially right about Cushings triade but this is called...Cushings Reflex...
Cushing reflex
The Cushing reflex (not to be confused with Cushing's triad) is a hypothalamic response to ischemia, usually due to poor perfusion (delivery of blood) in the brain.
The Cushing reflex consists of an increase in sympathetic outflow to the heart as an attempt to increase arterial blood pressure and total peripheral resistance, accompanied by bradycardia.
The ischemia activates the sympathetic nervous system, causing an increase in the heart's output by increasing heart rate and contractility along with peripheral constriction of the blood vessels. This accounts for the rise in blood pressure, ensuring blood delivery to the brain. The increased blood pressure also stimulates the baroreceptors (pressure sensitive receptors) in the carotids, leading to an activation of the parasympathetic nervous system, which slows down the heart rate, causing the bradycardia.
The Cushing reflex is usually seen in the terminal stages of acute head injury.
At first you will want to see f the patient has any improvement in LOC before further sedation.
Head injured patients are sedated all the time and some are placed in a drug induced coma to facilitate brain rest and limit brain irritation in an attempt to bide time until the welling decreases.
Even if a patient who is intubated and can't speak you can assess their LOC. An alert patient will write notes. Does the patient follow commands...not only grasp your hand for that can be reflex...will they let go or give you a thumbs up.
Do they localize noxious stimuli? Or do they only withdrawal to pain. Do the have abnormal response to noxious stimuli...
Abnormal posturing is an involuntary flexion or extension of the arms and legs, indicating severe brain injury. It occurs when one set of muscles becomes incapacitated while the opposing set is not, and an external stimulus such as pain causes the working set of muscles to contract. The posturing may also occur without a stimulus.
Since posturing is an important indicator of the amount of damage that has occurred to the brain, it is used by medical professionals to measure the severity of a coma with the Glasgow Coma Scale (for adults) and the Pediatric Glasgow Coma Scale (for infants).
The presence of abnormal posturing indicates a severe medical emergency requiring immediate medical attention.
Decerebrate and decorticate posturing are strongly associated with poor outcome in a variety of conditions
Thank you for taking the time to explain all of that! I don't generally like to ask questions about something that I haven't covered yet (and therefor may be able to figure it out once I cover the material), but I was curious I am still going to read over this in my text today, well, just because LOL. I will take a look at the links you posted, I am sure they'll be a great help! I love that [COLOR=#003366]♪♫ in my ♥ posted this, I have always found case studies to be a great way to learn.
smf0903
845 Posts
Oh gosh...well, critical care is next semester for me, but I will take a stab at it!
So, I would think that ICP would be monitored as well as spinal issues from the fall. I would think the biggest issues with a head trauma like that would be autonomic issues from the ICP and injury. I would think respiratory and temperature control are biggies, as well as watching for CSF leakage. I would also think BP control would be a big issue...blood loss (?) and diuretics to control the ICP could lead to big drop, but I did remember from some of the neuro we've covered that Cushing's triad was a late ICP sign. The pt could have dysrhythmias r/t damage to the brain.
I would think an antipyretic for temp control, some type of fluid replacement, and something for pain management. I would think that blood glucose would need to be monitored, as well as all things pituitary-related (SIADH, etc) because I would imagine any massive injury like that could mess with hypothalamus and/or pituitary. Possibly an anti-seizure med as well?
There's my spitballing LOL. I am sure I'll be thinking back on this post when we cover these kinds of injuries in critical care
I'll be watching for the follow-up to this!
edited to add...I thought of this but forgot to ask, at what GCS level do you discuss and make provisions for organ procurement, if it applies? (I know you said he was at a 6, but I can't imagine they leave all of that undealt with or at least discussed with a severe head injury and a low GCS score) I was wondering about that...