Blade's Cases

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look up the side-effects of cellcept. It lists increased INR as one.

I didn't know that before this case. I also didn't think about those darn antibodies, lupus anti-coagulants, etc. either BEFORE the case.

Blade

Lupus anti coagulants usually give you Isolated PTT elevation with normal INR.

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Lupus anti coagulants usually give you Isolated PTT elevation with normal INR.

I don't think she had a Lupus Anticoagulant. All I know for certain is that the CellCept was discontinued and that something rare caused her elevated INR.
Perhaps, I should have followed-up more with the Hematologist for an exact diagnosis.

Blade
 
Okay, case number 3 is a blend of dozens of actual cases. I see this type of case every week and have to deal with the issues routinely. Here it comes:

89 year old female with hip fracture. She lives in an "assisted facility" but gets around some on her own. She has mild Dementia but is oriented times three. The surgeon is planning on an elective Bipolar hip. The Anesthetic is up to you.

PMH

Mild Dementia
DJD/Arthritis
Chronic A. Fib
HTN
Hx lower GI bleed


PSH

Lap. Chole
Appendenctomy
Hernia Repair
Total Knee Replacement


Meds;

Plavix- Off 5 days (stopped because of GI bleed)
ASA- Off 5 days
Atenolol
Pepcid
Aricept


Labs:

EKG; A. Fib rate of 96
CXR; No acute disease
CBC; hgb= 9.5 Platelet Count 120,000
Coag: INR=1.1 PTT-WNL


Her son (age 62) shows up with her asking about "Regional" because of her Dementia. He is concerned about "worsening" her Dementia and asks me to do "anything possible" to keep her mental status near baseline. Her assisted living facility may not take her back if her Dementia becomes Severe.
Her son explains he can't take care of Mom and there is nobody else.

I see this type of case all the time. If it is not Plavix then it is INR=1.4 or it is INR=1.4 plus Plavix off 6 days. My hospital NOW has TEG available.

Blade
 
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I do a minimalistic GA on all these peopple, I avoid preop Midazolam and stick with propofol infusion and some Fentanyl intraop, very little inhaled agents if any.
I also do a Femoral nerve block for post op pain and they wake up as demented as they started, not worse.
 
I do a minimalistic GA on all these peopple, I avoid preop Midazolam and stick with propofol infusion and some Fentanyl intraop, very little inhaled agents if any.
I also do a Femoral nerve block for post op pain and they wake up as demented as they started, not worse.

Does the availability of TEG change your approach? If the TEG comes back normal would you do a Spinal?

Also, if the INR=1.4 and the patient is off Plavix for 5 days with NORMAL TEG would you do a Spinal?

If a Spinal is chosen as the anesthetic and minimal Propofol infusion is used along with No Midazolam does that "preserve" baseline mental status?
There are NO peer reviewed studies showing the type of anesthetic makes a difference in mental status. YET, MY EXPERIENCE SHOWS IT DOES MATTER TO A DEGREE WITH REGIONAL PRESERVING MENTAL STATUS THE BEST.

Plankton's GA technique is similar to my planned Regional in that Inhalational agents are avoided. Comments?

Finally, Does the use of TEG guarantee (with normal result) protection from a medical-legal standpoint if the patient develops an Epidural/Spinal hematoma?

Blade
 
This sounds like a patient to consider a continuous spinal anesthetic.

You could give one cc of 0.5% marcaine through a 20 gauge intrathecal cath (at L3-L4) over 30 seconds to a minute, wait 10-15 minutes, check the block. If the sensory block is lower than T10 give a half cc every 5 minutes until you’re satisfied with the block.

Although ASRA says you should wait 7 days with thienopyridines, but this technique is an option as it appears that antiplatelet therapy doesn’t increase the risk of spinal hematoma associated with spinal or epidural anesthesia (but the body of evidence on that is lacking, just a few reports which make this statement).
 
If her son asked you for a Spinal and requested blood products be given so a General Anesthetic could be avoided would you comply? This actually happened to me. The son, a 62 year old lawyer, asked me to give "products" to his Mom so she would be able to get a spinal. The lawyer was convinced based on his Friends' opinions that his Mom would be "much more likely to make it promptly back to the assisted living facility" after a Spinal.

I had the TEG results which were "normal" and normal Coags. So, what would you do?

1. Tell the son there is no evidence for GA vs. regional. So, you will NOT do the Spinal (He is the legal guardian of his mother). I guarantee he would be really pissed off at you .

2. Give the Platelets after writing a note in the chart and kindly advising against this approach. Then, do the spinal

3. Discuss the test results and NOT give any Platelets. Explain to him that the Platelets are not needed as you will do the spinal.

4. Have JPP tell the son to "get lost" as Grandma is going to get GA. Or, use Plankton's technique after explaining it to the son (No Peer reviewed evience for any technique being superior).


Blade
 
This sounds like a patient to consider a continuous spinal anesthetic.

You could give one cc of 0.5% marcaine through a 20 gauge intrathecal cath (at L3-L4) over 30 seconds to a minute, wait 10-15 minutes, check the block. If the sensory block is lower than T10 give a half cc every 5 minutes until you're satisfied with the block.

Although ASRA says you should wait 7 days with thienopyridines, but this technique is an option as it appears that antiplatelet therapy doesn't increase the risk of spinal hematoma associated with spinal or epidural anesthesia (but the body of evidence on that is lacking, just a few reports which make this statement).

Wait a Minute. I have SEEN what Plavix plus Lumbar puncture can do to a patient first hand. The result was not pretty and the guy still has a "bag" for his urine. The physician almost lost his license for doing the Lumbar puncture (a 22 gauge Q needle was used).

Plavix is NOT to be taken lightly and any Physician who uses a CUTTING NEEDLE on a patient on this medication is rolling the dice. When you COMBINE anti-platelet medication the effects of each one can be potentiated by the other.

Blade
 
Interesting discussion....& I obviously can't add anything to the anesthesia choices. But, I will add a few thoughts to the albuterol discussion, since this has changed in recent months.

Blade - you didn't mention if your albuterol tx is by nebulizer or mdi. Some RNs do nebulizers, but my institutions use RTs for that. There are very few non-HFC albuterol mdi's around....only if the wholesalers have them in stock. They'll be entirely out of production by Dec of this year....so..the $$ will be double.

Currently, HFC albuterol mdi's run about $0.40/gm (some more, some less depending on contracts). So, an mdi will "cost" the institution about $7.50 - small change. The newer non-HFC products "cost" about twice that & will become the routine product available. Except, someone has to give it - the rn or rt...or perhaps the pt himself. If the rn or rt administers the drug, the "cost" increases significantly due to the labor itself (figure approx 15 min/tx - $45/hr salary (includes benefits).....much more than the cost of the drug....without even including the labor costs you don't see....in the pharmacy.

Now....studies have shown approx 80% of an inhaled albuterol mdi is doposited in the oropharynx & subsequently absorbed into the GI tract then the blood. The albuterol is a mixture of the R-enantiomer which produces brochodilation & the S-enantiomer which can increase airway reactivity, oddly enough.

Its been shown that the kinetics of the R & S enantiomers is significantly different with the S enantiomer being retained preferentially in the lungs while the R-enantiomer tends to be more rapidly absorbed into the circulation via the GI route, although the portion which is actually delivered to the lungs is immediately active - thus rapid bronchodilation. The R-enantiomer portion absorbed into the lung peaks at 15-30 min & most of it is excreted within 30 min of the peak. The longer effects which are sometimes seen are due to the GI absorption of the R enantiomer - somewhat like giving oral albuterol. But...the S-enantiomer stays in the lung tissue and gets elminated much more slowly.

This gradual accumulation of the S-enantiomer, with slower elimination, is the basis for speculation as to why there tends to be a paradoxical increase in airway reactivity in those pts who regularly use (& abuse) albuterol inhalers.

So...not sure that this is even germain to your patient....just an interesting look at albuterol & why some like pretreatment & some don't. As a pharmacist - if you're going to give a pretx....I guess I'd rather you do it via an mdi. That actually "costs" less than the tubing, etc...which goes with the nebulizer even though the nebulized albuterol cost pennies. Since we're not reimbursed by line item used, even though it may cost my dept a bit more...I have to figure the cost of other depts as well.

There was just an interesting article on this in the NEJM. Non-CFC albuterol inhalers will be the norm and, because they are almost all still under patent, will cost significantly more than previous inhalers. The authors predicted an increase in healthcare expenditure of $1.2 Billion from this change alone; they also predicted massive amount of non-compliance with therapy among patients who cannot afford the new inhalers (which will likely lead to increased ED visits and admissions). Interestingly, they noted that Proventil, one of the CFC-free formulations, will cause positive readings on alcohol breathalizers for several minutes after administrations.
 
Wait a Minute. I have SEEN what Plavix plus Lumbar puncture can do to a patient first hand. The result was not pretty and the guy still has a "bag" for his urine. The physician almost lost his license for doing the Lumbar puncture (a 22 gauge Q needle was used).

Plavix is NOT to be taken lightly and any Physician who uses a CUTTING NEEDLE on a patient on this medication is rolling the dice. When you COMBINE anti-platelet medication the effects of each one can be potentiated by the other.

Blade

Definitely, nothing is taken lightly.
This is definitely an undefined area..... there is a report where Herbstreitand Peters (2005) gave platelets and then performed an uncomplicated spinal anesthetic in a patient with dual antiplatelet therapy because in their opinion the patient's disease state negated the general anesthetic option.
 
If the TEG and coags where normal...do the spinal. No need for FFP.
 
...This gradual accumulation of the S-enantiomer, with slower elimination, is the basis for speculation as to why there tends to be a paradoxical increase in airway reactivity in those pts who regularly use (& abuse) albuterol inhalers.

Hey sdn1977, just wondering if you know of any references re the above statement. It would make for an interesting topic on rounds tomorrow... Thanks.
 
Okay, case number 3 is a blend of dozens of actual cases. I see this type of case every week and have to deal with the issues routinely. Here it comes:

89 year old female with hip fracture. She lives in an "assisted facility" but gets around some on her own. She has mild Dementia but is oriented times three. The surgeon is planning on an elective Bipolar hip. The Anesthetic is up to you.

I have seen total hip cases done with a well placed fascia iliaca catheter. It is regional and avoids neuraxial techniques. A little propamine (prop with ketamine on top) might do the trick.

Hey, how come no one responded to my previous question about precedex on case #1? I guess the same could be applied in this case - fascia iliaca catheter with precedex.
 
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I have seen total hip cases done with a well placed fascia iliaca catheter. It is regional and avoids neuraxial techniques. A little propamine (prop with ketamine on top) might do the trick.

Hey, how come no one responded to my previous question about precedex on case #1? I guess the same could be applied in this case - fascia iliaca catheter with precedex.

Ketamine on an 86 Y/O demented patient might not be very elegant post op.
Precedex on an 86 Y/O dehydrated patient might cause the mother of all hypotensions.
:)
Precedex for bronchoscopy is definitely a good idea.
 
This sounds like a patient to consider a continuous spinal anesthetic.

You could give one cc of 0.5% marcaine through a 20 gauge intrathecal cath (at L3-L4) over 30 seconds to a minute, wait 10-15 minutes, check the block. If the sensory block is lower than T10 give a half cc every 5 minutes until you’re satisfied with the block.

Although ASRA says you should wait 7 days with thienopyridines, but this technique is an option as it appears that antiplatelet therapy doesn’t increase the risk of spinal hematoma associated with spinal or epidural anesthesia (but the body of evidence on that is lacking, just a few reports which make this statement).
If I had to do a spinal on a patient taking plavix for some really good reason the last thing I would do is place an indwelling catheter.
Think about it: Bigger needle, more trauma, continous risk of vessel trauma.......
 
If I had to do a spinal on a patient taking plavix for some really good reason the last thing I would do is place an indwelling catheter.
Think about it: Bigger needle, more trauma, continous risk of vessel trauma.......
Hey that's cool..............

Here is some info that is relevant and comes from Allen et al. (2002)

"
Horlocker et al performed a prospective study 4 years later in which 924 patients given spinal or epidural anesthesia were studied to determine the risk of hemorrhagic complications associated with regional anesthesia (20). In the study, 386 of the 924 patients took antiplatelet medications; no spinal hematomas were documented in these 386 patients, nor was the incidence of minor hemorrhagic complications increased. Other risk factors, including female sex, advanced age, history of excessive bruising/bleeding, hip surgery, continuous catheter anesthetic technique, large needle gauge, multiple needle passes, and moderate or difficult needle placement, were identified as significant risk factors.
Although antiplatelet medications by themselves may not increase the risk of complications associated with epidural or spinal anesthesia, there is some evidence that combining antiplatelet drugs with heparin therapy may induce spinal hematoma. Litz et al described a case in which a 63-year-old woman undergoing reimplantation of a right knee prosthesis developed a spinal hematoma (21). The patient had received one subcutaneous injection of low-molecular-weight heparin prophylactically and had a measured activated partial thromboplastin time of 33 seconds, a PT of 84%, and a platelet count of 151 × 103/μL. On the day of surgery, no heparin was given, and the epidural was placed preoperatively. Six hours after surgery, a dose of heparin was given. The patient complained of back pain, which was treated with 400 mg of ibuprofen. The patient continued to complain of back pain, so the epidural catheter was removed; 10 hours after removal, the patient developed voiding difficulties. Magnetic resonance imaging revealed an extensive spinal hematoma. Later it was revealed that the patient had regularly taken 500 mg of ibuprofen 4 times a day, and the last dose was 20 hours before surgery. The German Society of Anesthesiology recommends a free interval of 1 to 2 days after the last administration of a nonsteroidal agent and at least 3 days without aspirin before performing central neuraxial blocks. Litz et al echoed this recommendation."
 
Hey that's cool..............

Here is some info that is relevant and comes from Allen et al. (2002)

"
Horlocker et al performed a prospective study 4 years later in which 924 patients given spinal or epidural anesthesia were studied to determine the risk of hemorrhagic complications associated with regional anesthesia (20). In the study, 386 of the 924 patients took antiplatelet medications; no spinal hematomas were documented in these 386 patients, nor was the incidence of minor hemorrhagic complications increased. Other risk factors, including female sex, advanced age, history of excessive bruising/bleeding, hip surgery, continuous catheter anesthetic technique, large needle gauge, multiple needle passes, and moderate or difficult needle placement, were identified as significant risk factors.
"

Thanks for the Data.
 
Thanks for the Data.
Your welcome.

The POCD issue is also of interest to me as a neuroscientist, I thought I would provide this since it was brought up. I do think there is some form of POCD following GA but there is scant data.

Silverstein et al. (2007) Central nervous system dysfunction after noncardiac surgery and anesthesia in the elderly.

Regional versus General Anesthesia
It is intuitively appealing that general anesthesia, which specifically affects the brain, as compared with regional anesthesia, which affects primarily the spinal cord or peripheral nerves, would be associated with different rates of POCD. Beginning in 1980, a series of relatively small studies suggested that patients undergoing general anesthesia, but not neuraxial anesthesia, were at greater risk for POCD.34 In 1995, Williams-Russo et al.39 presented an adequately powered, prospective, randomized study of POCD that used standard neuropsychological instruments. This study compared the effect of epidural versus general anesthesia on the incidence of POCD in patients undergoing elective unilateral total knee replacement. Neurocognitive assessment was performed 1–7 days preoperatively (n = 262) and 1 week and 6 months (n = 231) postoperatively. Group mean scores for each of the 10 measures were compared between the two anesthesia groups, but no statistically significant differences were observed postoperatively. In addition, the proportions of patients exhibiting clinically important decrements for each test (defined by consensus) were compared. Overall, 5% of patients exhibited a decline in cognitive function 6 months after surgery, but no statistically significant differences were found between the anesthesia groups. As this was a comparative trial, there was no control group for reference. Recently, Wu et al.34 provided a comprehensive review of 24 studies that evaluated the choice of anesthesia and concluded that it does not influence the incidence of POCD.
 
truly an excellent informative case.
 
I had a little brain fart. FFP is not indicated in this case because the INR was normal. If anything Plavix would affect Platelet function which would not be helped by FFP. Anyway, since TEG and INR are NORMAL I just did the Spinal with a 22 gauge whitacre needle as the son requested.

If the INR was 1.4 and the TEG was normal would you do the Spinal?
What about INR of 1.6 (this assumes patient had been on Coumadin recently) and NO PLAVIX? My thresthhold is a INR of 1.5 and I don't exceed that number without FFP.

Blade

(I am going to correct the posts regarding FFP and change to Platelets:eek:)
 
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Your welcome.

The POCD issue is also of interest to me as a neuroscientist, I thought I would provide this since it was brought up. I do think there is some form of POCD following GA but there is scant data.

Silverstein et al. (2007) Central nervous system dysfunction after noncardiac surgery and anesthesia in the elderly.

Regional versus General Anesthesia
It is intuitively appealing that general anesthesia, which specifically affects the brain, as compared with regional anesthesia, which affects primarily the spinal cord or peripheral nerves, would be associated with different rates of POCD. Beginning in 1980, a series of relatively small studies suggested that patients undergoing general anesthesia, but not neuraxial anesthesia, were at greater risk for POCD.34 In 1995, Williams-Russo et al.39 presented an adequately powered, prospective, randomized study of POCD that used standard neuropsychological instruments. This study compared the effect of epidural versus general anesthesia on the incidence of POCD in patients undergoing elective unilateral total knee replacement. Neurocognitive assessment was performed 1–7 days preoperatively (n = 262) and 1 week and 6 months (n = 231) postoperatively. Group mean scores for each of the 10 measures were compared between the two anesthesia groups, but no statistically significant differences were observed postoperatively. In addition, the proportions of patients exhibiting clinically important decrements for each test (defined by consensus) were compared. Overall, 5% of patients exhibited a decline in cognitive function 6 months after surgery, but no statistically significant differences were found between the anesthesia groups. As this was a comparative trial, there was no control group for reference. Recently, Wu et al.34 provided a comprehensive review of 24 studies that evaluated the choice of anesthesia and concluded that it does not influence the incidence of POCD.


I am aware of this study and others like it to date. But, as a busy clinician I disagree with the results. I believe that the choice of Anesthetics do make a difference in the SHORT TERM and thus impacts patient care. I have been doing this long enough to WAIT OUT the literature to catch up with my theory. Although I firmly believe in the concept of peer reviewed literature EMPIRICAL EVIDENCE (especially a lot of it) does influence the way you practice. I am not advocating that my 'theory' be followed by anyone on this board. But like many things in Anesthesia all I have to do is wait long enough and see if I am correct.

As for the study looking at Anti-Platelet medication I don't believe that included CURRENT use of Plavix. Plavix is extremely potent and spinal anesthesia is a relative contraindication when a patient has been on the medication. The use of TEG for determining the choice of Anesthetic technique is relatively new. I am not aware of any sigificant studies PROVING a normal TEG means that you can disregard a patient being on Plavix in the recent past (7 days). Certainly, without TEG any provider who does a Spinal anesthetic AND gets a complication on a patient that has not been off PLavix for 7 days is going to get sued big time. There is also the chance the Medical Board (Nursing board in your case) may take your license. This would be GROSS NEGLIGENCE as I have seen this scenario first hand.
You also better have a good Malpractice policy because you will be paying the MAXIMUM and PRAYING the patient takes it.

Blade
 
I had a little brain fart. FFP is not indicated in this case because the INR was normal. If anything Plavix would affect Platelet function which would not be helped by FFP. Anyway, since TEG and INR are NORMAL I just did the Spinal with a 22 gauge whitacre needle as the son requested.

Blade

(I am going to correct the posts regarding FFP and change to Platelets:eek:)

To really see what is wrong with the platelets, your TEG machine has to have the special platelet mapping function, which I don't think very many hospitals use (according to the TEG rep). The reagents are very expensive and so most TEG users only can get a yes or no answer about platelets. The mapping function sounds very cool though. That function on the TEG may have helped in this clinical scenario.
 
I am aware of this study and others like it to date. But, as a busy clinician I disagree with the results. I believe that the choice of Anesthetics do make a difference in the SHORT TERM and thus impacts patient care. I have been doing this long enough to WAIT OUT the literature to catch up with my theory. Although I firmly believe in the concept of peer reviewed literature EMPIRICAL EVIDENCE (especially a lot of it) does influence the way you practice. I am not advocating that my 'theory' be followed by anyone on this board. But like many things in Anesthesia all I have to do is wait long enough and see if I am correct.

As for the study looking at Anti-Platelet medication I don't believe that included CURRENT use of Plavix. Plavix is extremely potent and spinal anesthesia is a relative contraindication when a patient has been on the medication. The use of TEG for determining the choice of Anesthetic technique is relatively new. I am not aware of any sigificant studies PROVING a normal TEG means that you can disregard a patient being on Plavix in the recent past (7 days). Certainly, without TEG any provider who does a Spinal anesthetic AND gets a complication on a patient that has not been off PLavix for 7 days is going to get sued big time. There is also the chance the Medical Board (Nursing board in your case) may take your license. This would be GROSS NEGLIGENCE as I have seen this scenario first hand.
You also better have a good Malpractice policy because you will be paying the MAXIMUM and PRAYING the patient takes it.

Blade
Just presenting options for discussion what I would do isn't necessarily what would be the options I present, I do think a single shot spinal is not inappropriate however, the continous spinal was presented b/c it is present in the literature....

In that case, another influence on my decision is the historical times, experience, and outcomes of the surgeon, nothing is performed in a vacuum
 
To really see what is wrong with the platelets, your TEG machine has to have the special platelet mapping function, which I don't think very many hospitals use (according to the TEG rep). The reagents are very expensive and so most TEG users only can get a yes or no answer about platelets. The mapping function sounds very cool though. That function on the TEG may have helped in this clinical scenario.

Here was my thought process about my decision to go ahead with the spinal.
First, the patient had been off Plavix and Aspirin for 5 days. Thus, you would expect some recovery of platelet function if not normal function. However, the overall platelet count was only 120,000 so this concerned me a bit.
But, the LABS and TEG were normal.

Second, the patient was a thin, elderly woman with a normal spine. I examined her back and other than the usual arthritis and degenerative disc disease I was confident that a paramedian spinal could easily be performed by me.

Third, I was going to use a non-cutting needle which should help a bit in decreasing trauma.

Fourth and finally, the patient was 89 years old and the son really wanted this technique. It is not like this person was going to be running a Marathon next week or any week for that matter.

Blade
 
So, I brought the little old lady to the O.R. She was placed in the lateral position and I did the Spinal with a 22 gauge Whitacre Needle. My local was Bupivicaine with Dextrose and the surgery took 80 minutes.

The patient stayed in the PACU for about an hour. Only a small amount of Propofol was used for the case (total 100 mg) with No Midazolam. I spoke with her son after Discharge from the PACU and he was very grateful. His mom seemed at baseline after the anesthetic but that doesn't mean she didn't have a rough time during her hospital stay.

I do know she made it back to the assisted living facility and her Dementia remained mild. The surgeon told me he appreciated my efforts in helping with this case.

Blade
 
Hey sdn1977, just wondering if you know of any references re the above statement. It would make for an interesting topic on rounds tomorrow... Thanks.

I think its in this article from 1999 - kinda old & I'm sure there is newer stuff, but I just got home from work & don't have time to research the newer articles before you need them ..... sorry:oops:.

Its a start though....

http://ajrccm.atsjournals.org/cgi/content/full/160/4/1136

Let me know if you want more & I'll work on it.
 
I think its in this article from 1999 - kinda old & I'm sure there is newer stuff, but I just got home from work & don't have time to research the newer articles before you need them ..... sorry:oops:.

Its a start though....

http://ajrccm.atsjournals.org/cgi/content/full/160/4/1136

Let me know if you want more & I'll work on it.


Okay,

So here is my question regarding Case number 1. My hospital has XOPENEX readily available by Resp. therapy. It was my understanding (correct me if I am wrong here) that CLINICALLY Xopenex offered no real advantage over generic Albuterol. In case number 1 I could have ordered Xopenex treatment instead of using the patient's own MDI. Do you think that may have had any value to DECREASING his risk of intra-op or post-operative resp. symptoms?

Due to cost I have only ordered Xopenex twice in the past 24 months and both times were in the PACU (patient had active wheezing and patient had history of Xopenex working better). Theoretically, the S Enantiomer of Albuterol (Xopenex) should show superiority to the generic which has S and R components. Comments?

Blade
 
Okay,

So here is my question regarding Case number 1. My hospital has XOPENEX readily available by Resp. therapy. It was my understanding (correct me if I am wrong here) that CLINICALLY Xopenex offered no real advantage over generic Albuterol. In case number 1 I could have ordered Xopenex treatment instead of using the patient's own MDI. Do you think that may have had any value to DECREASING his risk of intra-op or post-operative resp. symptoms?

Due to cost I have only ordered Xopenex twice in the past 24 months and both times were in the PACU (patient had active wheezing and patient had history of Xopenex working better). Theoretically, the S Enantiomer of Albuterol (Xopenex) should show superiority to the generic which has S and R components. Comments?

Blade

You may be interested in this, Kelly (2007) in a review found in Current Allergy and Asthma Reports suggested that the data was inconclusive in determining effectiveness of single isomer therapy.
 
Okay,

So here is my question regarding Case number 1. My hospital has XOPENEX readily available by Resp. therapy. It was my understanding (correct me if I am wrong here) that CLINICALLY Xopenex offered no real advantage over generic Albuterol. In case number 1 I could have ordered Xopenex treatment instead of using the patient's own MDI. Do you think that may have had any value to DECREASING his risk of intra-op or post-operative resp. symptoms?

Due to cost I have only ordered Xopenex twice in the past 24 months and both times were in the PACU (patient had active wheezing and patient had history of Xopenex working better). Theoretically, the S Enantiomer of Albuterol (Xopenex) should show superiority to the generic which has S and R components. Comments?

Blade

I thought studies showed a difference of 4 to 6 beat/min less with xopenex. No a huge difference for the cost. We have a ton of it around because of the albuterol shortage that happened a while back, so we were forced to stock the xopenex.
 
I think its in this article from 1999 - kinda old & I'm sure there is newer stuff, but I just got home from work & don't have time to research the newer articles before you need them ..... sorry:oops:.

Its a start though....

http://ajrccm.atsjournals.org/cgi/content/full/160/4/1136

Let me know if you want more & I'll work on it.

Thanks so much for the link. I am certainly able (and willing) to do the legwork, I just didn't know if there was a particularly notable/well-known study. Again, thanks.
 
Okay,

So here is my question regarding Case number 1. My hospital has XOPENEX readily available by Resp. therapy. It was my understanding (correct me if I am wrong here) that CLINICALLY Xopenex offered no real advantage over generic Albuterol. In case number 1 I could have ordered Xopenex treatment instead of using the patient's own MDI. Do you think that may have had any value to DECREASING his risk of intra-op or post-operative resp. symptoms?

Due to cost I have only ordered Xopenex twice in the past 24 months and both times were in the PACU (patient had active wheezing and patient had history of Xopenex working better). Theoretically, the S Enantiomer of Albuterol (Xopenex) should show superiority to the generic which has S and R components. Comments?

Blade

Just to clarify...Xopenex is the R-enantiomer - not the S.

There are a few points to consider here - first....the therapeutic one which was brought up by Jet - do you really need the prophylactic tx? I can't answer that one since I'm not in your shoes. You have the pts clinical situation & you use your best medical judgement - not in my realm - sorry:(.

However....this is what gets a bit confusing - the whole....do you use Xopenex or the albuterol inhaler situation. That is so dependent on the contractual status of the hospital pharmacy. Sometimes...drugs like this are "bundled" - which means....if you buy "this much" of XYZ drug - we'll throw in Xopenex at 1/3 the actual cost if you were to buy it otherwise.

I'm not so sure you'd actually know this information unless you went & asked the OR pharmacist (or any pharmacist you find around) - what is the formulary preference? Hopefully, on an annual basis, the pharmacy dept makes known what the formulary preference is of the many drug options available (proton pump inhibitors, fluoroquinolones, etc..)

Just because its available, doesn't mean its the best option - altho it could be if the dept got a good "deal".

In your case #1 - you were using this prophylactically (correct ME if I'm wrong...I'm tired....:() so an albuterol inhaler would probably be just fine. If it worked - great....if it didn't - you'd fix it with your medical interventions. I'm not sure you'd actually be able to tell where one stopped & the other began since you respond to what is occuring at that moment in time, whether it is as you extubate, in PACU or later.

For my actual opinion...since I advise the P&T committee on some issues - Xopenex does not offer an advantage to albuterol unless there is convincing evidence (ie the pt suffers severe bronchospasm secondary to albuterol tx) & that requires documentation by their respiratory physician....or if it becomes economically advantageous (money always speaks:p...)
 
There was just an interesting article on this in the NEJM. Non-CFC albuterol inhalers will be the norm and, because they are almost all still under patent, will cost significantly more than previous inhalers. The authors predicted an increase in healthcare expenditure of $1.2 Billion from this change alone; they also predicted massive amount of non-compliance with therapy among patients who cannot afford the new inhalers (which will likely lead to increased ED visits and admissions). Interestingly, they noted that Proventil, one of the CFC-free formulations, will cause positive readings on alcohol breathalizers for several minutes after administrations.

You're correct in that they do cost more. The reason is they had to develop a different delivery mechanism for the drug without the propellant. The generic "players" in the market did not see the economic benefit of doing this. Why? It is very, very, very expensive to go thru the process of getting an ANDA approved & generic manufacturers don't do this.

To bring everyone up to speed if you are "new" to inhalational medicine...the Montreal Protocol in 1996 was a world-wide agreement which all "first world" nations signed which gave a time limit to when CFC propellants would be eliminated from their products. Thats why you see Right Guard, hair spray & other products as "pumps" not as aerosols.

Thats also why you might have seen drugs like Serevent, Flovent, Pulmicort, etc...change their product. Those were all patent-protected so the $$$ expenditure on designing a new delivery system was compensated. (Now - you might not think it is that expensive - but...think of how much regulatory mess a company goes thru in the US - they have to go thru all that in each & every country. That does not include the change in manufacturing processes, packaging, education, etc..)

OK - so why was albuterol exempt - & it was. It was allowed to be exempt until Dec 2008 - a whole 12 years after this agreement..... The reason was because the drug was 1) very reliable 2) generic in every country 3) cheap. There really was no clear alternative...until Xopenex came along. But - that was really expensive (& still is!).

So - the 8 or 9 generic manufacturers of albuterol inhalers dropped out of the market slowly - we have now just 2. They can no longer distribute their product after Dec 2008. That is why there is sporadic shortages & it is substituted with Xopenex - therapeutically, they act the same. It is just with long term use, there might not be the buildup of the S-enantiomer which can cause bronchospasm.

Will it cost more - yes. In the outpt arena, if the insurance covers albuterol inhalers...they will cover albuterol CFC without a difference in copay (there is one generic - IVAX & 2 brand names - Proventil & Ventolin). The brand names are more expensive, but they have provided "incentives" in the form of the first one free & the next 3 at reduced prices. For hospitals...we absorb the cost difference just as we do with everything else since we are not paid for product...rather the drugs are part of the drg.

However, there is not yet sufficient production to covert all albuterol pts worldwide to CFC free product. We hope there will be by Dec 2008!

Never heard about positive breathalyzer tests - I don't know what they "test" for.....
 
At the U of Chicago we have a study going comparing fent/midaz vs dexmedetomidine for FOBI sedation. I suspect the outcome will show they're about the same but one is dramatically more expensive.

The dex ought to be much more effective as well as expensive.
 
Yes,

Plankton's technique is a great idea and I would be willing to bet that the patient's mental status after propofol GA is the same as after Spinal plus propofol.

We need more studies in this area especially comparing varying techniques.

Blade
 
Another case I had the good fortune of being involved with recently.


A 49 year white male coming emergently to the O.R. with perforated viscous.
He has been "sick" for three days at home but came to the E.R. only three hours ago.

Vitals:

temp-101 F
HR- A. Fib rate= 156
BP 80/50
RR= 24

PMH

Tobacco 2ppd for 30 years

PSH
None

Meds:
None

Labs:

CBC: WBC 17,000 Hg 17.9 Platelet 336,000
Chem-7: WNL
EKG A. Fib rate-154
CXR: No acute Disease


He has one antecubital I.V. (20 gauge) from the E.R. He has received about 2 liters of LR so far when you get him into the O.R.

What is your plan? What is your approach? The surgeon is slow and will take 3-4 hours for the case.

Blade
 
Another case I had the good fortune of being involved with recently.


A 49 year white male coming emergently to the O.R. with perforated viscous.
He has been "sick" for three days at home but came to the E.R. only three hours ago.

Vitals:

temp-101 F
HR- A. Fib rate= 156
BP 80/50
RR= 24

PMH

Tobacco 2ppd for 30 years

PSH
None

Meds:
None

Labs:

CBC: WBC 17,000 Hg 17.9 Platelet 336,000
Chem-7: WNL
EKG A. Fib rate-154
CXR: No acute Disease


He has one antecubital I.V. (20 gauge) from the E.R. He has received about 2 liters of LR so far when you get him into the O.R.

What is your plan? What is your approach? The surgeon is slow and will take 3-4 hours for the case.

Blade

This was a really interesting case. Come on, Mil MD, JPP or Plankton play along here it gets better.
 
Hello everybody, I am new to the site

Preop
main issues are the pt's HR, afib, decreased BP with a perfed viscous (sepsis, hypovolemia, or rate related?) and the fact that this is an emergency case that needs to be done now. Also what is perfed ulcer vs. diverticulum

First I would optimize volume status the try to control the pt's rate with cardizem as tolerated by BP, bolus with caution and then start drip, start neo if needed, I would try not to cardiovert unless BP's are falling and there was no other choice.

It would be nice to know why the pt is in afib, but you are not going to get a definitive answer in time to do the case. History would help but regardless of the answer I would still be going to the OR. An echo would be nice esp. if any abnormalities were found on exam but in my hospital the echo would be done and read by sometime next week.

I would start a CVL, aline, and try to remind someone to place a foley

Induction
Etomidate/sux/narcotic of choice as tolerated/tube in an RSI fashion, I would avoid lido for fear of increasing the rate

Maint.
Volatile of choice, O2, NDMR of choice

Emergence
evaluate for extubation as we do for every case, keeping in mind recent ABG's and the general operative course, I think this pt would be well served in an ICU post op regardless of vent status
 
I would also consider a cordis or at least a couple of large gauge IVs in. Some way to pump this guy full of fluid since he is still likely extremely dehydrated.

I would strongly consider cardioverting this guy if his blood pressure doesnt respond to the fluid resuscitation. It would be nice to get some history indicating that the afib is a recent occurence of course, but if his blood pressure is borderline now, it sure isnt going to improve on induction. Basically, I would think the risk of severe hypotension outweighs the potential risks from systemic emboli. Having said that, I would probably drop a TEE when the case settles down to see if theres any clot in the atria or LAE.

2 large gauge IVs, awake aline, lots of fluid. RSI (ketamine or etomidate + succ). cordis after induction. Pray the BP stays up. If not start on phenylephrine/norepi drip. If BP still low consider vasopressin. Have epi available just in case.

Depending on how this guys BP reacts to induction and inhaled we might just have to get by on some versed and narcotics.
 
The guy is septic, hypovolemic and in atrial fibrillation as a result.
We have to address these three elements:
First get good IV access, I think a triple lumen should be good enough. and start dumping crystalloids in.
Start an A line, send a blood gas.
Place Foley.

I would do these things in the unit or in holding before going to the OR.
If his hemodynamics don't improve after 2-3 liters of crystalloids or if the CVP starts rising too fast I would try to cardiovert him, but most likely the AFIB will slow down or go back to sinus spontaneously once you start catching up with fluids. I would also add Phenylephrine to the game early to work on the septic component of the problem.
Treat his pain which could be an important contributer to his AFIB.
I Know it might be voodoo but I still give Digoxin in these patients if I decide to just slow the ventricular rate, and small increments of Esmolol.
By that time I am hoping he is already getting wide spectrum ATBX.
Once the patient is more stable:
BP is better, starting to make urine, Afib is back to sinus or ventricular rate is slower, we can go to the OR.
RSI: Etomidate + Sux, ETT, NG tube, Continue fluids + Pressors.
The key word here is Fluids.
the rest is routine.
 
The guy is septic, hypovolemic and in atrial fibrillation as a result.
We have to address these three elements:
First get good IV access, I think a triple lumen should be good enough. and start dumping crystalloids in.
Start an A line, send a blood gas.
Place Foley.

I would do these things in the unit or in holding before going to the OR.
If his hemodynamics don't improve after 2-3 liters of crystalloids or if the CVP starts rising too fast I would try to cardiovert him, but most likely the AFIB will slow down or go back to sinus spontaneously once you start catching up with fluids. I would also add Phenylephrine to the game early to work on the septic component of the problem.
Treat his pain which could be an important contributer to his AFIB.
I Know it might be voodoo but I still give Digoxin in these patients if I decide to just slow the ventricular rate, and small increments of Esmolol.
By that time I am hoping he is already getting wide spectrum ATBX.
Once the patient is more stable:
BP is better, starting to make urine, Afib is back to sinus or ventricular rate is slower, we can go to the OR.
RSI: Etomidate + Sux, ETT, NG tube, Continue fluids + Pressors.
The key word here is Fluids.
the rest is routine.

The longer this guy is septic, the higher his mortality risk.

I'd bring him to the back, rapid sequence like Plankton described above.

Triple lumen/NGT/A line while they're prepping the belly. The A line can be done after you are prepped and draped if they're ready before its done...dont make'em wait for you....drape away then work on the A line.

Start pouring in crystalloid.....you may give 7-10 liters during a case like this.

The A fib isnt gonna kill this guy. The sepsis resultant from the perfed viscus will.

So I agree with Plankton on just about everything above....except that I wouldnt do anything to this guy preoperatively....wouldnt wait for fluid to be in, etc....I'd do everything to him intraoperatively..use the little IV to go to sleep with, then do all your stuff simultaneous to the surgeon prepping....since the only thing thats gonna make him better is a steel blade to his belly.

And the faster the better (for him).

Cardioversion wont do anything for him until the underlying etiology is fixed.
 
The longer this guy is septic, the higher his mortality risk.

I'd bring him to the back, rapid sequence like Plankton described above.

Triple lumen/NGT/A line while they're prepping the belly. The A line can be done after you are prepped and draped if they're ready before its done...dont make'em wait for you....drape away then work on the A line.

Start pouring in crystalloid.....you may give 7-10 liters during a case like this.

The A fib isnt gonna kill this guy. The sepsis resultant from the perfed viscus will.

So I agree with Plankton on just about everything above....except that I wouldnt do anything to this guy preoperatively....wouldnt wait for fluid to be in, etc....I'd do everything to him intraoperatively..use the little IV to go to sleep with, then do all your stuff simultaneous to the surgeon prepping....since the only thing thats gonna make him better is a steel blade to his belly.

And the faster the better (for him).

Cardioversion wont do anything for him until the underlying etiology is fixed.


You can do the resuscitation in the OR but I would rather be ahead of the game a little or he will not tolerate induction and PPV.
 
THanks for the response. All excellent. Here is what I did for the guy.

I brought him to the O.R. ASAP. I would have liked more time for evaluation or just fluid replacement but IMPATIENT surgeons (he had his partner) led to my going right to the O.R.

The bowel was the likely source of sepsis (suspected perforated diverticulum). He was not distended so I skipped the NG tube pre-induction.
What do you think about that move? Next, I gave 100 ug Neosynephrine and placed the A-Line. Then, RSI with Etomidate and SUX. After induction Central line X 2 (cordis 8.5F and triple lumen) and LITERS of fluid.
He tolerated induction okay and only needed a little NEO. After 6 liters of LR I decided to address the HR of 140. I loaded with Digoxin (probably B.S.) and gave 20 mg Esmolol. He tolerated this well and HR slowed to 120 ( A.fib).
I gave 2 liters more LR and 500 Hextend. I slowly gave Lopressor in 1 mg increments up to 5 mg. The HR slowed to 105 (still A.fib).

The surgeons resected the bowel for the next 3 hours. I placed NG tube and the urine output was pretty good. After 3 hours the HR started to increase again to 140 and BP started to drop 78/48. I started NEO drip but changed to Norepi infusion. At this point total fliuds were 11 liters LR plus 500 ml Hextend. CVP=7 The case ended and I took the patient to the PACU.
The time now is 0100 and here are the vitals in Pacu on the Vent.

BP= 83/54
HR= 146
SAt= 99%
ABG= 7.31/31/135 BE= -8 on 50%
Hgb= 11.9 Platelets 180,000 INR=1.4 PTT-WNL

Urine output is still good 200 cc/hr and CVP=6.

Now what? The patient told me prior to induction NO HEART PROBLEMS and no history of A.Fib? The surgeon wants me to handle the situation and remember it is 0100.

Blade
 
I Know it might be voodoo but I still give Digoxin in these patients if I decide to just slow the ventricular rate, and small increments of Esmolol.

RSI: Etomidate + Sux, ETT, NG tube, Continue fluids + Pressors.
The key word here is Fluids.
the rest is routine.

There is an cardiothoracic anesthesiologist that I have worked with that uses digoxin all the time. Unfortunately, I think this drug fell out of favor a few years back so us newbies don't get to see it's use much. It seemed like when I was an intern in 2000, we used it a ton. I wish I had more experience with it.

If I were doing this case, I would also place a RIC (rapid infusion catheter) if I didn't use the 8.5 french introducer in the neck. They are very handy to have with very little downside to placement.

My take....

Induction ...whatever didn't kill him. The specific agent probably doesn't matter as much as how it is used. I would absolustely avoid etomidate. Maybe scopalamine with some other stuff mixed in as an RSI.

Fluid management - what it takes to get CVP 8-12, UOP to .5ml/kg. I would check frequent SvO2 and use 70% as a goal. I think also I would use colloids a lot ....yes...despite their lack of evidence... but there is some soft evidence that it is better in preventing abdominal compartment syndrome, which this gentlemen will be at high risk for post op if he gets a ton of fluid, which he most likely will.

Norepi would be my choice for a vassopressor. My Ionotrope, if needed, would be dopamine - to keep my MAP >60. Keeping in mind his tacchycardia, if fluids would not reduce the rate first, my vassopressor of choice would be neosynephrine - trying to avoid beta stimulation. Vassopressin certainly has shown to be a great choice in sepsis, but I don't know if it is a good choice in this situation, knowing that vassopressin causes gut vasoconstriction.

I would try to maintain a hematocrit of 30%, and I would check lactates often.

If I struggled with blood pressure, I would have a low trigger to give steroids as his adrenals are most certainly suppressed.

The big question is whether or not to give Xigris. I don't know on this. What do other say?
 
THanks for the response. All excellent. Here is what I did for the guy.

I brought him to the O.R. ASAP. I would have liked more time for evaluation or just fluid replacement but IMPATIENT surgeons (he had his partner) led to my going right to the O.R.

The bowel was the likely source of sepsis (suspected perforated diverticulum). He was not distended so I skipped the NG tube pre-induction.
What do you think about that move? Next, I gave 100 ug Neosynephrine and placed the A-Line. Then, RSI with Etomidate and SUX. After induction Central line X 2 (cordis 8.5F and triple lumen) and LITERS of fluid.
He tolerated induction okay and only needed a little NEO. After 6 liters of LR I decided to address the HR of 140. I loaded with Digoxin (probably B.S.) and gave 20 mg Esmolol. He tolerated this well and HR slowed to 120 ( A.fib).
I gave 2 liters more LR and 500 Hextend. I slowly gave Lopressor in 1 mg increments up to 5 mg. The HR slowed to 105 (still A.fib).

The surgeons resected the bowel for the next 3 hours. I placed NG tube and the urine output was pretty good. After 3 hours the HR started to increase again to 140 and BP started to drop 78/48. I started NEO drip but changed to Norepi infusion. At this point total fliuds were 11 liters LR plus 500 ml Hextend. CVP=7 The case ended and I took the patient to the PACU.
The time now is 0100 and here are the vitals in Pacu on the Vent.

BP= 83/54
HR= 146
SAt= 99%
ABG= 7.31/31/135 BE= -8 on 50%
Hgb= 11.9 Platelets 180,000 INR=1.4 PTT-WNL

Urine output is still good 200 cc/hr and CVP=6.

Now what? The patient told me prior to induction NO HEART PROBLEMS and no history of A.Fib? The surgeon wants me to handle the situation and remember it is 0100.

Blade

Your case sounds somewhat similar to one presented in a 2005 edition of Anesthesia and Analgesia where they used Landiolol (very short acting) beta antagonist for treatment. It appears to make logical sense to increase diastolic filling time to improve cardiac output especially since your patient reported no previous cardiac history.

Successful Management of Tachycardic Atrial Fibrillation in a Septic Patient with Landiolol

Yoshida et al., 2005

Landiolol was started at the rate of 5 µg · kg-1 · min-1 for 15 min, and was maintained 2 to 3 µg · kg-1 · min-1. In 15 min after landiolol infusion, HR and PA decreased and stabilized at around 80 bpm, around 30 mm Hg, respectively. SBP increased and stabilized at about 120 mm Hg. This case demonstrates that landiolol attenuated the tachycardia-induced low cardiac stroke volume and stabilized the hemodynamics in a patient with sepsis. Landiolol was reported to cause neither excessive hypotension nor cardiac decompression and is thought to be useful for treating tachycardia in sepsis patients.
 
THanks for the response. All excellent. Here is what I did for the guy.

I brought him to the O.R. ASAP. I would have liked more time for evaluation or just fluid replacement but IMPATIENT surgeons (he had his partner) led to my going right to the O.R.

The bowel was the likely source of sepsis (suspected perforated diverticulum). He was not distended so I skipped the NG tube pre-induction.
What do you think about that move? Next, I gave 100 ug Neosynephrine and placed the A-Line. Then, RSI with Etomidate and SUX. After induction Central line X 2 (cordis 8.5F and triple lumen) and LITERS of fluid.
He tolerated induction okay and only needed a little NEO. After 6 liters of LR I decided to address the HR of 140. I loaded with Digoxin (probably B.S.) and gave 20 mg Esmolol. He tolerated this well and HR slowed to 120 ( A.fib).
I gave 2 liters more LR and 500 Hextend. I slowly gave Lopressor in 1 mg increments up to 5 mg. The HR slowed to 105 (still A.fib).

The surgeons resected the bowel for the next 3 hours. I placed NG tube and the urine output was pretty good. After 3 hours the HR started to increase again to 140 and BP started to drop 78/48. I started NEO drip but changed to Norepi infusion. At this point total fliuds were 11 liters LR plus 500 ml Hextend. CVP=7 The case ended and I took the patient to the PACU.
The time now is 0100 and here are the vitals in Pacu on the Vent.

BP= 83/54
HR= 146
SAt= 99%
ABG= 7.31/31/135 BE= -8 on 50%
Hgb= 11.9 Platelets 180,000 INR=1.4 PTT-WNL

Urine output is still good 200 cc/hr and CVP=6.

Now what? The patient told me prior to induction NO HEART PROBLEMS and no history of A.Fib? The surgeon wants me to handle the situation and remember it is 0100.

Blade

Try to cardiovert him.
Put him on Neo or Norepi drip.
 
There is an cardiothoracic anesthesiologist that I have worked with that uses digoxin all the time. Unfortunately, I think this drug fell out of favor a few years back so us newbies don't get to see it's use much. It seemed like when I was an intern in 2000, we used it a ton. I wish I had more experience with it.

If I were doing this case, I would also place a RIC (rapid infusion catheter) if I didn't use the 8.5 french introducer in the neck. They are very handy to have with very little downside to placement.

My take....

Induction ...whatever didn't kill him. The specific agent probably doesn't matter as much as how it is used. I would absolustely avoid etomidate. Maybe scopalamine with some other stuff mixed in as an RSI.

Fluid management - what it takes to get CVP 8-12, UOP to .5ml/kg. I would check frequent SvO2 and use 70% as a goal. I think also I would use colloids a lot ....yes...despite their lack of evidence... but there is some soft evidence that it is better in preventing abdominal compartment syndrome, which this gentlemen will be at high risk for post op if he gets a ton of fluid, which he most likely will.

Norepi would be my choice for a vassopressor. My Ionotrope, if needed, would be dopamine - to keep my MAP >60. Keeping in mind his tacchycardia, if fluids would not reduce the rate first, my vassopressor of choice would be neosynephrine - trying to avoid beta stimulation. Vassopressin certainly has shown to be a great choice in sepsis, but I don't know if it is a good choice in this situation, knowing that vassopressin causes gut vasoconstriction.

I would try to maintain a hematocrit of 30%, and I would check lactates often.

If I struggled with blood pressure, I would have a low trigger to give steroids as his adrenals are most certainly suppressed.

The big question is whether or not to give Xigris. I don't know on this. What do other say?


Why no Etomidate?
 
Try to cardiovert him.
Put him on Neo or Norepi drip.


Agree. Unstable narrow complex tacchycardia = cardiovert.

You could try some amiodarone to continue in the ACLS algorithym. I think a TEE would be helpful, even better, just throw the probe on the outside - TTE just to take a look.

CVP = 6? Maybe I would give some Albumin.

Why no Etomidate?

I am worried about adrenal suppression in an already adrenal-compromised patient. I know they say it happens with infusions, but I also have seen discussions in the literature about single doses causing significant suppression. Since there are other drugs that can accomplish the same thing, I would use those.

Any thought to Xigris?
 
(
).

The surgeons resected the bowel for the next 3 hours. I placed NG tube and the urine output was pretty good. After 3 hours the HR started to increase again to 140 and BP started to drop 78/48. I started NEO drip but changed to Norepi infusion. At this point total fliuds were 11 liters LR plus 500 ml Hextend. CVP=7 The case ended and I took the patient to the PACU.
The time now is 0100 and here are the vitals in Pacu on the Vent.

BP= 83/54
HR= 146
SAt= 99%
ABG= 7.31/31/135 BE= -8 on 50%
Hgb= 11.9 Platelets 180,000 INR=1.4 PTT-WNL

Urine output is still good 200 cc/hr and CVP=6.

Now what? The patient told me prior to induction NO HEART PROBLEMS and no history of A.Fib? The surgeon wants me to handle the situation and remember it is 0100.

Blade


Good job so far on keeping him alive up to this point.

Now I would try to determine whether the unstable hemodynamics are because of a malignant rhythm or because of hypovolemia or because of sepsis or because of cardiomyopathy.

1. Feel his feet. If the feet are warm, it's because he's septic. And he needs vasopressor. Go with phenylephrine because norepi has some beta action and it'll continue to aggravate the arrythmia. Plus, phenylephrine will bring the HR down in and of itself and might even promote "eu-rhythmia."

2. If the feet are cold, it's either because he's hypovolemic, or in cardiogenic shock. What's the CVP? It looks to be 6-8? Start volume loading to a CVP of 12+. After that, if feet are still cold, drop in a TEE and look for another cause of shock: cardiogenic -- poor contractility from sepsis or acidemia? obstructive -- tamponade?

3. Once one and two are done, load with amio 150 x 2 and start amio infusion. Start antibiotics. Poor response to pressors? Start dexamethasone 4-10 mg q6h and send off cort-stim test. Optimize vent settings to protect lungs.

4. Relax. Good job. Now you just need a tincture of time. He'll either get better or get worse. There's nothing more you can do. If he gets better, congratulations. If he doesn't: you win some, you lose some.
 
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