Case to share

[funkyfaroh]

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Ok, so after reading and benefiting from all the advice and info on this forum, I think its about time to share and take the opportunity to learn from the folks on here. I am a CA-1 and have just completed my first couple of months. This past friday, I was involved in a case that both intrigued me and scared the living sh$t out of me.....here's how it goes.

20 year old male with extended family (at least 3 kids already) has a tragic accident at the repair shop as he's filling up an 18 wheeler tire. The tire explodes as he's putting pressure into it and in the process loses his LLE, left eye, multiple facial and extremity fractures. He survives. He is now a resident at our level 1 trauma hospital and has had multiple surgeries for his injuries. Most of the have been washouts and internal fixations. When it comes to my turn to assume care, he is in the STICU, having recently started CCHD with renal insufficiency, on a levafed drip, recently titrated down to 10 mcg/kg/min. At baseline, he is lethargic, follows commands, but obviously septic and struggling to survive. In the OR, i continue to the levafed drip, utilize his 2 sources of Central venous access (RSC, RIJ) and give Isoflurane via his tracheostomy site. (6 cuffed down in unit, inflated for surgery). So, throughout the case, things seem to be running smoothly. I maintain his MAP, his pressures remain normotensive throughout the whole case....and I start to breathe again.

Towards the end of the case, the patient is now breathing spontaneously and I am preparing for extubation (disconnecting the circuit from the trach). I take off the tape from his eyes, and subsequently assess what stage of sleep he's in. Left eye is prosthesis, right eye.....fixed and dilated. HOLY HELL MOTHER OF ALL THINGS SCARY AS FREAKING MONKEYS CA-1 DEATH WOA IS ME.

Yes, that is what crosses my mind at that moment. What did I do? Did I do anything? Was it like that before? Did I botch my pre-op? I look at the blood gases from the case. This is from top of my head so bear with me. 1)7.35/190/glu 55/k-3.5/LA 3.2( this was at beginning of case after I placed arterial line) Based on the pre-op report, he needed calcium, mg, and glucose. I replaced the mag over 2 hrs, the calicium intraop and the glucose with D50, 12.5g x2 over the case.
2)7.3/ca corrected, glucose corrected LA 4.5

I was in the room for the majority of the case on my own, and one thing I did not do (doh!) is give bicarb. I was so focused on the BP's being on point, etc....

So, to summarize and try to wrap things up, we take him straight to CT scanner from ICU post-op to rule out whatever must have happened to him. I toiled over it all night, checked the scan myself and found that the CT was negative, he began to respond to commands again, and apparently his pupil started reacting again. WHEW.

Ok, bombs away. I'm here to learn.

 

[pgg]

on a levafed drip

Levophed.

obviously septic

You didn't say what surgery he was having. If he was obviously septic, I'm assuming this was a washout or some procedure to address the source of his infection.

I look at the blood gases from the case. This is from top of my head so bear with me. 1)7.35/190/glu 55/k-3.5/LA 3.2

That's an odd way to present lab data. I take it the 190 was his PaO2? Usually an ABG is related as pH / PCO2 / PO2 / bicarb (calculated not measured value) / base excess. Other than mild hypoglycemia I don't see much to get too worked up over in those labs.

one thing I did not do (doh!) is give bicarb.

Why do you think he needed bicarb? There really aren't many times when a patient needs bicarb and this patient's pH was 7.35. If he already has a prosthetic eye then this isn't happening immediately post-injury when the renal failure might be due to rhabdo and alkalinization of urine might help. I can't think of any other reason off the top of my head why a non-acidotic trauma patient might benefit from bicarb.

On the surface it doesn't sound like you did anything wildly inappropriate, but the story isn't real clear, either.

 

[funkyfaroh]

sorry for the incomplete info and spelling errors. His second pH value was 7.3 and his lactic acid level went from 3.2 to 4.5. That is why I thought he might have needed bicarb.

 

[militarymd]

Norepinephrine at 10 mcg/kg/min??????

 

[funkyfaroh]

yes, he was having a washout case to isolate and treat his source of infection.

 

[funkyfaroh]

thanks for the correction mil.
It was 0.10 intially in the OR and the max I had to go to was 0.50

 

[funkyfaroh]

I figured maybe they felt comfortable enough with me to let me work on a harder case. I wanted to be up to the challenge, you know?

 

[militarymd]

thanks for the correction mil.
It was 0.10 intially in the OR and the max I had to go to was 0.50

that's still a lot of vasoactive drug...I hope they weren't trying to REMOVE fluid during dialysis.

As for dilated pupils....could have been anything...Have you ever dropped some norepinephrine into someone's eye and see what happens?

 

[funkyfaroh]

No I haven't, but I'm sure its a quite a sight. (no pun intended.)

 

[funkyfaroh]

I was quite relieved though when he began to respond post operative and improve. Since then, its been more of a exercise for me to learn from my cases, especially that have been difficult for my level.

 

[ProRealDoc]

Ok, so after reading and benefiting from all the advice and info on this forum, I think its about time to share and take the opportunity to learn from the folks on here. I am a CA-1 and have just completed my first couple of months. This past friday, I was involved in a case that both intrigued me and scared the living sh$t out of me.....here's how it goes.

20 year old male with extended family (at least 3 kids already) has a tragic accident at the repair shop as he's filling up an 18 wheeler tire. The tire explodes as he's putting pressure into it and in the process loses his LLE, left eye, multiple facial and extremity fractures. He survives. He is now a resident at our level 1 trauma hospital and has had multiple surgeries for his injuries. Most of the have been washouts and internal fixations. When it comes to my turn to assume care, he is in the STICU, having recently started CCHD with renal insufficiency, on a levafed drip, recently titrated down to 10 mcg/kg/min. At baseline, he is lethargic, follows commands, but obviously septic and struggling to survive. In the OR, i continue to the levafed drip, utilize his 2 sources of Central venous access (RSC, RIJ) and give Isoflurane via his tracheostomy site. (6 cuffed down in unit, inflated for surgery). So, throughout the case, things seem to be running smoothly. I maintain his MAP, his pressures remain normotensive throughout the whole case....and I start to breathe again.

Towards the end of the case, the patient is now breathing spontaneously and I am preparing for extubation (disconnecting the circuit from the trach). I take off the tape from his eyes, and subsequently assess what stage of sleep he's in. Left eye is prosthesis, right eye.....fixed and dilated. HOLY HELL MOTHER OF ALL THINGS SCARY AS FREAKING MONKEYS CA-1 DEATH WOA IS ME.

Yes, that is what crosses my mind at that moment. What did I do? Did I do anything? Was it like that before? Did I botch my pre-op? I look at the blood gases from the case. This is from top of my head so bear with me. 1)7.35/190/glu 55/k-3.5/LA 3.2( this was at beginning of case after I placed arterial line) Based on the pre-op report, he needed calcium, mg, and glucose. I replaced the mag over 2 hrs, the calicium intraop and the glucose with D50, 12.5g x2 over the case.
2)7.3/ca corrected, glucose corrected LA 4.5

I was in the room for the majority of the case on my own, and one thing I did not do (doh!) is give bicarb. I was so focused on the BP's being on point, etc....

So, to summarize and try to wrap things up, we take him straight to CT scanner from ICU post-op to rule out whatever must have happened to him. I toiled over it all night, checked the scan myself and found that the CT was negative, he began to respond to commands again, and apparently his pupil started reacting again. WHEW.

Ok, bombs away. I'm here to learn.

Do you keep a penlight or flashlight handy?

 

[Idiopathic]

sick dude, it happens. i cant highlight anything you did wrong, except maybe allow your levophed dose to get to 0.5 mcg/kg/min. I dont really have a "max dose" in mind when i give norepi but then again ive never had someone on over 30 mcg/min before.

so if this patient is truly septic then he needs good source control, you told us that they had actually titrated his norepi down to 0.1 per kg (probably down from the ICU max of 0.2) which leads you to believe that he was improving. you should remember that the dose of norepi is typically in mcg/min (i.e. "10 mcg/min" or in fractions of mcg/kg/min, i.e. "0.1 mcg/kg/min" especially when presenting to attendings or giving report)

i think using a PA cath or lidco might have helped you in the OR. Its likely this patient needed volume more than that much norepi. and running that high a dose would probably cause your pupillary issues.

and i dont think many of us would give bicarb to treat a isolated rise in lactate, unless you have severe acidemia.

 

[Fastrach]

Dilated pupil at the end of surgery on a previously healthy 20 y/o dude with a bunch of ortho injuries makes me wonder if he has received adequate narcotic for the case. Did he?

 

[Idiopathic]

i thought that too, but if he is requiring that much norepi to maintain a BP then likely the intrinsic catechols are so depleted that i doubt the pain response is as significant. certainly a possible cause also.

 

[SexPanther]

i thought that too, but if he is requiring that much norepi to maintain a BP then likely the intrinsic catechols are so depleted that i doubt the pain response is as significant. certainly a possible cause also.

Dude, nice to see you've decided to post again but seriously, could you please capitalize the start of your sentences. It's like I'm reading a 7 year old's thoughts.

 

[SexPanther]

Dude...Did they really stick you with a septic, hemodynamically unstable ICU patient, as a CA1, only few months in? That's harsh.

This isn't that uncommon of a CA-1 case, at least in my experience.

It is nice to get some clinical discussion going, I enjoy reading everybody's takes on things.

 

[coprolalia]

pgg,

I read ya. 😉

Sniff... sniff...

-copro

P.S. 2 mcg/kg/min of levophed is... well... the patient's pretty much ****ed if you're at that much, let's just say. Our institutional "titration limit" in our ICUs is 0.5 mcg/kg/min. The physician has to write a specific order if you expect the nurse to titrate above that to maintain a certain MAP. And, again, the solution to pollution is dilution... plus, adequate fluid resuscitation, not giving bicarb. Then again, if you actually were at 10 mcg of levo, I can understand why the lactate was climbing... no splanchnic bloodflow! ($0.02)

 

[Idiopathic]

our ICU limit is 0.2 but ive exceeded that in special cases

 

[funkyfaroh]

Thanks for the feedback. I knew that some of the responses would be critical of my lack of experience (kid not knowing doses of norepi, etc) and understanding, but I know that its these kind of clinical discussions that facilitate learning. At the end of the day, I know the transformation from being a rookie to a seasoned Anesthesiologist takes time, effort, and dedication. I'm enjoying the ride.

 

[fakin' the funk]

Norepinephrine, what a cool drug - how many others can you titrate across a 100-fold dosing range (at our joint it's 0.2 - 20 mcg/min).

Sounds like a fun case - young dude with a good heart already vented/trach'd and in the ICU so if you want to help the MAP via the preload route, you could pound in the fluids and wean down some pressors - it sounds like there was room to do so.

I think the "wayyy too much norepi" explanation for the pupil was a good one. I'm trying to think of other ways to test that theory clinically (other tests/physical exam findings) but can't off the top of my head.

 

[periopdoc]

Don't worry about it. I am a CT Fellow, and If you were a member of the private forum you would see that the other day I made a vasopressin dosing mistake when writing a post.

Now, I know how to dose Vaso. I use it every D^^^^ day. Furthermore, I am always giving the residents a hard time when they mistakenly say that they are giving X mcg/kg/min of Vaso. However, I posted the units wrong. The funniest part was when Blade gently reminded me to recheck my dosing, I defended the correct dosing, but didn't go back to see that I had written incorrect dosing units. To make matters worse I made the error a second time cause I was in a hurry. Doh.

So far, that is the closest I have come to an actual medication error, but embarrassing nonetheless.

- pod

 

[SexPanther]

Sometimes doses of the numerous drugs we use can be difficult to remember. I recommend the Anesthesia and Critical Care reference sheet from www.accrs.com.

I have the pocket size version that fits into my back scrub pocket - it can be very handy.

 

[6stringsdown]

Dilated pupil at the end of surgery on a previously healthy 20 y/o dude with a bunch of ortho injuries makes me wonder if he has received adequate narcotic for the case. Did he?

I'm just wondering how this correlates. I have never seen this scenario b/c of inadequate narcs. I'm by no means an expert, but quite curious.

 

[6stringsdown]

1. ortho injuries with inadequate narcs causes pain
2. pain causes sympathetic activation
3. sympathetic activation causes pupil dilation

but unilaterally?

 

[Idiopathic]

1. ortho injuries with inadequate narcs causes pain
2. pain causes sympathetic activation
3. sympathetic activation causes pupil dilation

this is true, although im sticking with the massive NE doses as my first choice 😉

 

[6stringsdown]

Ok, so after reading and benefiting from all the advice and info on this forum, I think its about time to share and take the opportunity to learn from the folks on here. I am a CA-1 and have just completed my first couple of months. This past friday, I was involved in a case that both intrigued me and scared the living sh$t out of me.....here's how it goes.

20 year old male with extended family (at least 3 kids already) has a tragic accident at the repair shop as he's filling up an 18 wheeler tire. The tire explodes as he's putting pressure into it and in the process loses his LLE, left eye, multiple facial and extremity fractures. He survives. He is now a resident at our level 1 trauma hospital and has had multiple surgeries for his injuries. Most of the have been washouts and internal fixations. When it comes to my turn to assume care, he is in the STICU, having recently started CCHD with renal insufficiency, on a levafed drip, recently titrated down to 10 mcg/kg/min. At baseline, he is lethargic, follows commands, but obviously septic and struggling to survive. In the OR, i continue to the levafed drip, utilize his 2 sources of Central venous access (RSC, RIJ) and give Isoflurane via his tracheostomy site. (6 cuffed down in unit, inflated for surgery). So, throughout the case, things seem to be running smoothly. I maintain his MAP, his pressures remain normotensive throughout the whole case....and I start to breathe again.

Towards the end of the case, the patient is now breathing spontaneously and I am preparing for extubation (disconnecting the circuit from the trach). I take off the tape from his eyes, and subsequently assess what stage of sleep he's in. Left eye is prosthesis, right eye.....fixed and dilated. HOLY HELL MOTHER OF ALL THINGS SCARY AS FREAKING MONKEYS CA-1 DEATH WOA IS ME.

Yes, that is what crosses my mind at that moment. What did I do? Did I do anything? Was it like that before? Did I botch my pre-op? I look at the blood gases from the case. This is from top of my head so bear with me. 1)7.35/190/glu 55/k-3.5/LA 3.2( this was at beginning of case after I placed arterial line) Based on the pre-op report, he needed calcium, mg, and glucose. I replaced the mag over 2 hrs, the calicium intraop and the glucose with D50, 12.5g x2 over the case.
2)7.3/ca corrected, glucose corrected LA 4.5

I was in the room for the majority of the case on my own, and one thing I did not do (doh!) is give bicarb. I was so focused on the BP's being on point, etc....

So, to summarize and try to wrap things up, we take him straight to CT scanner from ICU post-op to rule out whatever must have happened to him. I toiled over it all night, checked the scan myself and found that the CT was negative, he began to respond to commands again, and apparently his pupil started reacting again. WHEW.

Ok, bombs away. I'm here to learn.

Outta curiosity, i'm guessing the eye was taped before you arrived, and didn't know it was a prosthesis?

 

[6stringsdown]

He had an eye injury on the other side (fake eye). Re-read the first post.

uh, yea.. never mind. sympathetics can fit.

 

[Dirtball]

If you called me to the room after taking the tape off and presented the above , I would ask you if you thought he needed some narcotic. Give 50ugs , then if the pupil moves, you may have your answer. Great forum, I found it a couple months back searching for board review info. Don't worry it will become alot more fun a few years down the road when the anxiety level decreases. I am about 18-20,000 cases ahead of you and really do enjoy my work. ..Keep asking questions, I still learn things weekly.

 

[urge]

I have noticed some pts have dilated pupils by the end of the case during stage 2. They revert back to normal in a few min.

Stop squealing like a ...... A botched neuro exam during wake up is meaningless.

 

[SleepIsGood]

Lactic Acidosis--> likely from hypoperfusion.


Guy is a young man. Put a CVP....POUR...i mean POUR fluids into while looking at the CVP and following trends. Then given HCO3 if that's not correcting anything.

 

[Idiopathic]

Lactic Acidosis--> likely from hypoperfusion.


Guy is a young man. Put a CVP....POUR...i mean POUR fluids into while looking at the CVP and following trends. Then given HCO3 if that's not correcting anything.

yeah i think weve stressed the need for fluids in this septic patient maxed on norepi, but im not sure id treat elevated LA in someone with a normal pH with bicarb

 

[Narcotized]

I can't think of any other reason off the top of my head why a non-acidotic trauma patient might benefit from bicarb.

You might consider it for non-acidotic hyperkalemia, though I realize that wasn't a presenting problem in this particular case.

 

[Narcotized]

This isn't that uncommon of a CA-1 case, at least in my experience.

Cool, let me know what hospital you are referring to... so I can wear an ID bracelet saying "Mr. Ambulance Driver, in case of severe trauma with sepsis within a few months of July 1, keep driving past this hospital." 😱😱 🙂

 

[dhb]

Lactic Acidosis--> likely from hypoperfusion.


Guy is a young man. Put a CVP....POUR...i mean POUR fluids into while looking at the CVP and following trends. Then given HCO3 if that's not correcting anything.

CVP is not affected by fluid loading nor is the trend...

 

[pgg]

You might consider it for non-acidotic hyperkalemia, though I realize that wasn't a presenting problem in this particular case.

Yeah, good point, forgot the obvious indication. 🙂

 

[fakin' the funk]

CVP is not affected by fluid loading nor is the trend...

Do explain. Still trying to wrap my head around how to apply the whole high-capacitance high-compliance central venous system stuff to actual clinical fluid mgmt

 

[proman]

Does central venous pressure predict fluid responsiveness? A systematic review of the literature and the tale of seven mares.
Marik PE, Baram M, Vahid B.
Chest. 2008 Jul;134(1):172-8
Division of Pulmonary and Critical Care Medicine, Thomas Jefferson University, 834 Walnut St, Suite 650, Philadelphia, PA 19107, USA. [email protected]

BACKGROUND: Central venous pressure (CVP) is used almost universally to guide fluid therapy in hospitalized patients. Both historical and recent data suggest that this approach may be flawed. OBJECTIVE: A systematic review of the literature to determine the following: (1) the relationship between CVP and blood volume, (2) the ability of CVP to predict fluid responsiveness, and (3) the ability of the change in CVP (DeltaCVP) to predict fluid responsiveness. DATA SOURCES: MEDLINE, Embase, Cochrane Register of Controlled Trials, and citation review of relevant primary and review articles. Study selection: Reported clinical trials that evaluated either the relationship between CVP and blood volume or reported the associated between CVP/DeltaCVP and the change in stroke volume/cardiac index following a fluid challenge. From 213 articles screened, 24 studies met our inclusion criteria and were included for data extraction. The studies included human adult subjects, healthy control subjects, and ICU and operating room patients. DATA EXTRACTION: Data were abstracted on study design, study size, study setting, patient population, correlation coefficient between CVP and blood volume, correlation coefficient (or receive operator characteristic [ROC]) between CVP/DeltaCVP and change in stroke index/cardiac index, percentage of patients who responded to a fluid challenge, and baseline CVP of the fluid responders and nonresponders. Metaanalytic techniques were used to pool data. DATA SYNTHESIS: The 24 studies included 803 patients; 5 studies compared CVP with measured circulating blood volume, while 19 studies determined the relationship between CVP/DeltaCVP and change in cardiac performance following a fluid challenge. The pooled correlation coefficient between CVP and measured blood volume was 0.16 (95% confidence interval [CI], 0.03 to 0.28). Overall, 56+/-16% of the patients included in this review responded to a fluid challenge. The pooled correlation coefficient between baseline CVP and change in stroke index/cardiac index was 0.18 (95% CI, 0.08 to 0.28). The pooled area under the ROC curve was 0.56 (95% CI, 0.51 to 0.61). The pooled correlation between DeltaCVP and change in stroke index/cardiac index was 0.11 (95% CI, 0.015 to 0.21). Baseline CVP was 8.7+/-2.32 mm Hg [mean+/-SD] in the responders as compared to 9.7+/-2.2 mm Hg in nonresponders (not significant). CONCLUSIONS: This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVP/DeltaCVP to predict the hemodynamic response to a fluid challenge. CVP should not be used to make clinical decisions regarding fluid management.

 

[fakin' the funk]

This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVP/DeltaCVP to predict the hemodynamic response to a fluid challenge. CVP should not be used to make clinical decisions regarding fluid management.

So doesn't this make Rivers et al, with CVP as the very first parameter to target, a load of $hit?

 

[proman]

So doesn't this make Rivers et al, with CVP as the very first parameter to target, a load of $hit?

The authors of the review article would think so. They do address it in the article. I'm not sure I agree.

 

[dhb]

There are countless studies on the issue and it appears clear that CVP is a very bad marker for volume status. I attended the panel on this subject at the ASA and all the panelist where on board with this.

We have been substituting pressure (CVP, PAOP) for volume for a long time and it's time that everybody recognize that it is wrong.

 

[Robert Loblaw]

Do explain. Still trying to wrap my head around how to apply the whole high-capacitance high-compliance central venous system stuff to actual clinical fluid mgmt

simple. give propofol to your fasting patients. simple. give neo to your hypotensive patients after giving propofol. simple. start putting all your fasting patients with a-lines in trendelenberg...and observe. the venous capacitance system is the MOST important system for actual clinical fluid mgmt.

pouring crystalloid into anyone is NEVER a good idea. total body hypovolemia is rarely the clinical answer to the question of hypotension, and it is not the pathology in sepsis--vaso/venodilation is. as such, i think that a judicious crystalloid/colloid PLUS early vasopressor therapy to address the vasodilatory shock is a better strategy. this also avoids the problem of having to diurese 45 pounds of saline to someone!

 

[hoyden]

There are countless studies on the issue and it appears clear that CVP is a very bad marker for volume status. I attended the panel on this subject at the ASA and all the panelist where on board with this.

We have been substituting pressure (CVP, PAOP) for volume for a long time and it's time that everybody recognize that it is wrong.

If you combine the values of CVP/LA/septic Hx/extreme doses of vasopressors/ABGs - you may conclude that a massive fluid volume is needed( to improve oxygen delivery to the tissues it is blood, which might be needed)...
But you can make that conclusion without CVP as well.

Just a remark - a multitrauma septic patient( in a need of high doses of vasoactive drugs) in the ICU has 2 central lines and no arterial line?

 

[funkyfaroh]

If you combine the values of CVP/LA/septic Hx/extreme doses of vasopressors/ABGs - you may conclude that a massive fluid volume is needed( to improve oxygen delivery to the tissues it is blood, which might be needed)...
But you can make that conclusion without CVP as well.

Just a remark - a multitrauma septic patient( in a need of high doses of vasoactive drugs) in the ICU has 2 central lines and no arterial line?

Great point. So when I went to go see the patient, the ICU nurse had told me that for some reason they lost the arterial line and that I had come for the patient before the ICU team had rounded on him for the day. So, I placed the arterial line and took him to the OR immediately after. I've already gained a lot reading all the posts. Thanks.