Mock Oral Exam

Started by Noyac
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Noyac said:
What turned out to be the cause b/c so far nobody is even close on this one?
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Honestly - I do not know. I suspect it was a kind of withdrawal - guy happened to be on every possible narcotic, I do suspect - on supplemental "recreational drugs" as well. In order to undergo surgery was probably abstinent for couple of days.
I have searched the internet on the issue and found this - http://www.jcafulltextonline.com/article/S0952-8180(03)00056-4/abstract
 
hoyden said:
Honestly - I do not know. I suspect it was a kind of withdrawal - guy happened to be on every possible narcotic, I do suspect - on supplemental "recreational drugs" as well. In order to undergo surgery was probably abstinent for couple of days.
I have searched the internet on the issue and found this - http://www.jcafulltextonline.com/article/S0952-8180(03)00056-4/abstract
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I didn't check out your link but mostly your post has fallen behind. This thread has started to move rapidly.
 
Noyac said:
You may be right but tell us why you would choose to give it.
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Metabolic acidosis and clinical symptoms ---> MH has to be high on your suspicion list, especially since this kid has never had surgery and anesthesia before and dantrolene is a pain to dilute and needs to be given early.
 
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Noyac said:
I didn't check out your link but mostly your post has fallen behind. This thread has started to move rapidly.
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yeah, I can see it. Since I am still preparing for orals - I do not read the thread to the end and try to answer before )))) forgive my falling behind - it is still kind of mock oral - FOR ME 🙂
 
hoyden said:
Metabolic acidosis and clinical symptoms ---> MH has to be high on your suspicion list, especially since this kid has never had surgery and anesthesia before and dantrolene is a pain to dilute and needs to be given early.
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Please explain the metabolic acidosis.
 
Noyac said:
Please explain the metabolic acidosis.
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7.38/43/102/26/ 0.1 - your ABG

7.38 - is slightly acidic, 43 - is normal; 26 - is normal
slightly acidotic pH is not caused by excess of CO2 or base deficit, therefore, some other acidic components cause it. LA is the most probable cause.
 
hoyden said:
7.38/43/102/26/ 0.1 - your ABG

7.38 - is slightly acidic, 43 - is normal; 26 - is normal
slightly acidotic pH is not caused by excess of CO2 or base deficit, therefore, some other acidic components cause it. LA is the most probable cause.
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There's probably not much significance about 7.38. There is no one exact normal pH just like there is no one exact normal temperature of 98.6. Normal falls in ranges. Anything between 7.35 and 7.45 is probably insignificant.
 
Narcotized said:
There's probably not much significance about 7.38. There is no one exact normal pH just like there is no one exact normal temperature of 98.6. Normal falls in ranges. Anything between 7.35 and 7.45 is probably insignificant.
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You are right, it is almost insignificant. However, given the scenario while taking the oral board I would still put MH as # 1 on my list.

MH does not have to be a full-blown catastrophic event from the very beginning. It has various degrees of expression. Which only means it has to be very high on your list of suspicion.
 
OK, now that you got me curious and I caught up on the last 50 posts, real life or board exam, I'd be crapping in my pants if I didn't give Dantrolene. I'm surprised you held off. So is MH what he had? Without rereading MH, I thought I remembered rising CO2 to be the typical initial presentation. This one started slow, but when he picked up steam in the PACU with the acidosis and temp spike, I'm not playing hero for the exact diagnosis; I'm shotgunning like a Family Practitioner and pushing Dantrolene.
 
Noyac said:
arterial ABG 7.38/43/102/26/ 0.1
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Noyac said:
I-Stat (venous) is 7.21/68/20/-1/27 K 4.0 Ca 5.0 Glu 105
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Something's up with the iStat or the patient changed dramatically. A VBG pH should be almost the same as an ABG pH. One study found

Pearson's product-moment correlation coefficients between arterial and venous values were as follows: pH, 0.913; Pco(2), 0.921; and HCO(3), 0.953. The mean differences (and 95% CIs) between arterial and venous samples were as follows: pH, 0.036 (0.030-0.042); Pco(2), 6.0 (5.0-7.0) mm Hg; and HCO(3), 1.5 (1.3-1.7) mEq/L. The mean differences (+/- 2 standard deviations) were greater than the minimum clinically important differences identified in the survey.

CJEM. 2002 Jan;4(1):7-15.
 
Very good you guys. I honestly couldn't remember the difference btw venous and arterial BG's at 0100 in the morning. I thought they should be more closely related but I wasn't certain. I knew that when the venous BG was sent I had been supporting his resp effort with a jaw lift so I deducted that it could be CO2 retention due to obstruction. I also noticed that as I turned off the vent in the OR to get him breathing at the end of the case his CO2 rose to 52 real fast but it was very easy to get back down to the 30's with some assistance. I normally wouldn't have worried and would have let it rise in hopes of him responding by breathing but for some reason I wanted to see if I could get it down easily which was the case therefore I thought maybe it's not MH. So I was thinking MH even during the case when I turned off the gas 1/2 thru the case and when I tried to see how easy it was to control the CO2. But I was never convinced.

Proman, you are right, the pt changed dramatically. He went from "posturing" to A&OX3 in a matter of 10 minutes.

Narc, I guess I wasn't crapping my pants b/c he looked pretty good aside from his tendency to boil at any minute.

So like Hoyden stated, MH does not have to be a full blown catastrophic event from the start.

But it can be a full blown event at any time within the next 24-36 hours.
 
Noyac said:
So like Hoyden stated, MH does not have to be a full blown catastrophic event from the start.

But it can be a full blown event at any time within the next 24-36 hours.
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So what finally happened? This is more suspenseful than The Hills series finale tonight.
 
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My guess is that this kid did not have MH. As far as I know, active cooling does not terminate an MH crisis. It needs to be terminated at the cellular level. Ryanodine receptor/sarcoplasmic reticulum and it's release of calcium need to be addressed by Dantrolene (prevents the calcium-induced release of calcium within myocyte) if MH is present. Also, Noy said he could easily bring his etCO2 down. But as mentioned above, it does not have to be an acute event.

Definitely interested in halo-caffeine contracture test is this kid.
 
Ok, enough with the suspense. I sent him to the ICU with a temp of around 102. We kept the cooling blanket on him and around 4am his temp started to rise again while under the cooling blanket. We packed him in ice and started mixing the dantrolene. The big surprise is that the dantrolene was incredibly easy to mix. Just like mixing Ancef and we all know we get plenty of practice doing that. I understand that last year a new form of easy mixing dantrolene was made available. Apparently we have that one. I gave him a little over 1mg/kg bolus and was ready to give the next 1mg/kg dose but he started to shiver and finally said he felt cold. I remember that dantrolene works rapidly but we barely got the first 20 mg in when he started to shiver. His temp was 102.8 and dropped to 102.6 rapidly but slowed after that. He felt cold so I had the ice removed and the cooling blanket remained until he got down to 100.0 about 4 hrs later. If you wait til they are normothermic you will over shoot and they will be hypothermic shortly after. The cooling blanket never really went back on and I continued to bolus him every 6 hrs with 1mg/kg dantrolene.

I learned a good lesson here. Everything went well and nobody in the hospital had ever seen a case of MH so the outside consults were nonexistent. I learned to give dantrolene as soon as you truly suspect MH. I would say this was when he was in the PACU for me. They tolerate the stuff very well. I thought I was going to have to re-intubate him but he never felt very weak. With that being said, it wiped out his appetite completely, and he had a very difficult time standing yesterday. Hopefully, he feels better today.
 
So does everyone think this was MH? His ABG's never got out of whack. His CPK spiked at 1800 (not terribly high). His urine did get very dark and then stopped coming all together. His temp was definitely challenging to control but not as challenging as I would have thought. There are many ways for MH to present. I think if this had been a more practical presentation I would have treated it much sooner but things may have turned out worse, much worse.:boom:
 
Freakn' strong work Noy. Thanks for sharing. I was nearly sure it wasn't MH until he spiked up again and ulitmately got the dantrolene. I'm with Plank. Could or could not be MH. But you did the right thing fo sure.

How did you determine when to stop bolusing 1mg/kg of dantrolene q6hrs? What was your end point? Did you try and flush him out? Renal failure?

Huge bonus case. :prof::claps:
 
sevoflurane said:
Freakn' strong work Noy. Thanks for sharing. I was nearly sure it wasn't MH until he spiked up again and ulitmately got the dantrolene. I'm with Plank. Could or could not be MH. But you did the right thing fo sure.

How did you determine when to stop bolusing 1mg/kg of dantrolene q6hrs? What was your end point? Did you try and flush him out? Renal failure?

Huge bonus case. :prof::claps:
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Kidneys responded well to the 5 mg lasix dose in the PACU. The dantrolene has manitol in it so that maintained his UOP from then on.

The protocol is to give the initial bolus of dantrolene at first signs of MH and then start an infusion or repeat boluses every 6 hrs for 36 hrs. I stopped at 36 hrs and the ICU nurses were nervous that he would spike again. His temp went up to 99.8 and they were calling me like crazy. I held off and it didn't get any higher. We are 24 hrs post last dose dantrolene now and looking good.
 
WOW, thanks Noyac for sharing. Great case and I suspect it is MH. Not only can it manifest without full-blown picture, but can even be very mild the first time the pt gets exposed to triggers - obviously depends on the subtype of the defect and the dose and time of exposure to the triggers.
 
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Noyac said:
COuld be. But it would be ice to know whether your MH is due to a dystrophy or just MH.
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While there is a definitive link between MH and CCD, one has never been proven between MH and muscular dystrophy.

The concern with unrecognized muscular dystrophies is rhabdomyolysis and life-threatening hyperkalemia which can occur with inhalational agents with and without succinylcholine administration.

These findings are often similar to those seen with MH but a definitive link has not been shown...yet:

A & A October 2009 vol. 109 no. 4 1043-1048

Malignant Hyperthermia and Muscular Dystrophies
Harshad Gurnaney, MBBS, MPH*†, Amanda Brown, MD*† and Ronald S. Litman, DO*†
+ Author Affiliations

From the *Department of Anesthesiology and Critical Care Medicine, The Children’s Hospital of Philadelphia; and †Department of Anesthesiology and Critical Care Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania.
Address correspondence and reprint requests to Harshad Gurnaney, MBBS, MPH, Department of Anesthesiology and Critical Care Medicine, The Children’s Hospital of Philadelphia, 34th St. and Civic Center Blvd., Philadelphia, PA 19104-4399. Address e-mail to [email protected].

Abstract
BACKGROUND: Patients with muscular dystrophy have been reported to experience a variety of life-threatening complications during and after general anesthesia. We performed a systematic analysis to define the spectrum of anesthetic-related complications in patients with muscular dystrophy, with an emphasis on malignant hyperthermia susceptibility.

METHODS: A literature search was undertaken using multiple search engines and the appropriate articles were reviewed by the authors to determine anesthetic-associated complications in patients with muscular dystrophy. Of all the types of muscular dystrophy, Duchenne muscular dystrophy (DMD) and Becker dystrophy (BD) represent nearly all the anesthesia-related reports.

RESULTS: Anesthetic complications in patients with DMD and BD include intraoperative heart failure, inhaled anesthetic-related rhabdomyolysis (absence of succinylcholine), and succinylcholine-induced rhabdomyolysis and hyperkalemia.

CONCLUSION: We did not find an increased risk of malignant hyperthermia susceptibility in patients with DMD or BD compared with the general population. However, dystrophic patients who are exposed to inhaled anesthetics may develop disease-related cardiac complications, or rarely, a malignant hyperthermia-like syndrome characterized by rhabdomyolysis. This latter complication may also occur postoperatively. Succinylcholine administration is associated with life-threatening hyperkalemia and should be avoided in patients with DMD and BD.
 
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