Crazy Case today

[nitecap]

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29 yr old primigravada at 26wks gestation. Saw OB a month ago with HA. OB sent her home saying all looked ok. Comes in one week later with intense HA, weakness to bilat Lower ext and htn. Diagnosed with TB menengitis and now 3 wks later is paraplegic and is in for a VP shunt stat. Is extubated now but was intubated about 2wks ago with resp distress and pneumonia . Its a little hectic CRNA is preoxygenating while MD prepping drugs. Pt K 3.0, pH 7.33, BP marginal 95/68, HR ST 120's sats 98%, in AAO and speaking though cant move lower ext.

Anesthesiologist pushes drugs for induction STP mg/kg, fent 2mcg/kg, Suxs .8mg/kg. CRNA intubates all is straight. 2 minutes later pt goes into Vfib, compressions started, no freaking gel in room for defib pabbles, surgeon defibs on straight skin x 2 shocks, pt back in ST 120's, chest burnt pretty bad from shock. Fetal hrt tones Nml, baby ok, mom Awake and talking.

What went wrong here? A few theories thrown around are :

Cardiology thinks it was suxs induced hyperkalemia though anesthesia is aurguing that K was only 3.0 so dont think it was that. Post incident K 3.7.

Since BP was marginal some are saying STP dropped BP low enough to cause ischemia that causes VFib. Anesthesia admits not getting accurate cuff pressures with inductionbut claiming he chose gold stanard OB induction agent. Cardio disagreeing saying moms heart is young and healthy and that he thinks should could have compensated well enough.

What do you think? Would you have used this drug selection? What would you have done diff? The paraplegia was over 2 wks old but the K was 3.0 so is this an issue.

Just curious to see what others thought, noboby seemed to agree on anything and all just wanted to blame this incident on things that made them look the least bad.

 

[Noyac]

It was the sux!

Large upregulation of receptors at the NM junctions in the recently paralyzed pt led to large K release and therefore, V. Fib.

I am surprised that she came back that easily though. Not usually the case in my understanding although I have never seen it cause I don't know anyone that would have given sux in a case like this.

 

[nitecap]

I thought similarly since you really dont know just how many extra jxnl receptors there really are. Also not sure if all the harmonal issues of pregnancy would cause even greater up regulation of these extra jxnls.

As far as the Gamma Nicotinic xtra jxnl. I understand that it has poorer conductance but a longer opening time. So the K effluxes when the suxs depolarizes increasing plasma K. Though a jump from a K of 3.0 to a level that causes dysrhthmias as such seems like it would have to be a large increase in K.

Also immediately after the incident they drew labs and the K was 3.7. Did the K go back intracellularly that fast?

 

[jetproppilot]

29 yr old primigravada at 26wks gestation. Saw OB a month ago with HA. OB sent her home saying all looked ok. Comes in one week later with intense HA, weakness to bilat Lower ext and htn. Diagnosed with TB menengitis and now 3 wks later is paraplegic and is in for a VP shunt stat. Is extubated now but was intubated about 2wks ago with resp distress and pneumonia . Its a little hectic CRNA is preoxygenating while MD prepping drugs. Pt K 3.0, pH 7.33, BP marginal 95/68, HR ST 120's sats 98%, in AAO and speaking though cant move lower ext.

Anesthesiologist pushes drugs for induction STP mg/kg, fent 2mcg/kg, Suxs .8mg/kg. CRNA intubates all is straight. 2 minutes later pt goes into Vfib, compressions started, no freaking gel in room for defib pabbles, surgeon defibs on straight skin x 2 shocks, pt back in ST 120's, chest burnt pretty bad from shock. Fetal hrt tones Nml, baby ok, mom Awake and talking.

What went wrong here? A few theories thrown around are :

Cardiology thinks it was suxs induced hyperkalemia though anesthesia is aurguing that K was only 3.0 so dont think it was that. Post incident K 3.7.

Since BP was marginal some are saying STP dropped BP low enough to cause ischemia that causes VFib. Anesthesia admits not getting accurate cuff pressures with inductionbut claiming he chose gold stanard OB induction agent. Cardio disagreeing saying moms heart is young and healthy and that he thinks should could have compensated well enough.

What do you think? Would you have used this drug selection? What would you have done diff? The paraplegia was over 2 wks old but the K was 3.0 so is this an issue.

Just curious to see what others thought, noboby seemed to agree on anything and all just wanted to blame this incident on things that made them look the least bad.

Sux with new onset paraplegia isnt a great idea. The risk of stimulating upregulated-extrajunctional K receptors with potential concominant cardiac sequalae far outweighs the (minimal) risk of aspiration in a parturient. Risk vs benefit. Important to remember.

Whats the risk of a parturient aspirating during a general anesthetic, even if you have to gently ventilate her for a minute or so?

Very very low.

Whats the risk of cardiac-sequalae if you give sux to a new onset paraplegic?

Much higher than the aspiration risk.

Use a non-depolarizer.

 

[militarymd]

I would not have used succinylcholine on this patient, BUT from what you described, I don't think it was hyperkalemic cardiac arrest.


Hyperkalemia does not cause V-fib, and if it is truly hyperkalemic related v-fib, shocking is NOT going to bring you back quickly.

I've only seen this once....the ECG progress from NSR to sinusoidal over the course of a few minutes....and it takes a bit of time before the K+ goes back into the cells....and during that time, you're really not resuscitatable.

There are some articles published by a Navy institution back in the 70's or 80's where they caused a sailor to arrest repeatedly before they figured it all out...serial ecgs, serial blood draws...etc.

Anyways, just my 2 cents....what you described is not what I have personally seen in sux related hyperkalemic arrest.

 

[militarymd]

I would go with STP induced hypotension....what dose was used?

 

[nitecap]

STP dose was 4mg/kg, not sure exact weight of pt.

 

[stephend7799]

29 yr old primigravada at 26wks gestation. Saw OB a month ago with HA. OB sent her home saying all looked ok. Comes in one week later with intense HA, weakness to bilat Lower ext and htn. Diagnosed with TB menengitis and now 3 wks later is paraplegic and is in for a VP shunt stat. Is extubated now but was intubated about 2wks ago with resp distress and pneumonia . Its a little hectic CRNA is preoxygenating while MD prepping drugs. Pt K 3.0, pH 7.33, BP marginal 95/68, HR ST 120's sats 98%, in AAO and speaking though cant move lower ext.

Anesthesiologist pushes drugs for induction STP mg/kg, fent 2mcg/kg, Suxs .8mg/kg. CRNA intubates all is straight. 2 minutes later pt goes into Vfib, compressions started, no freaking gel in room for defib pabbles, surgeon defibs on straight skin x 2 shocks, pt back in ST 120's, chest burnt pretty bad from shock. Fetal hrt tones Nml, baby ok, mom Awake and talking.

What went wrong here? A few theories thrown around are :

Cardiology thinks it was suxs induced hyperkalemia though anesthesia is aurguing that K was only 3.0 so dont think it was that. Post incident K 3.7.

Since BP was marginal some are saying STP dropped BP low enough to cause ischemia that causes VFib. Anesthesia admits not getting accurate cuff pressures with inductionbut claiming he chose gold stanard OB induction agent. Cardio disagreeing saying moms heart is young and healthy and that he thinks should could have compensated well enough.

What do you think? Would you have used this drug selection? What would you have done diff? The paraplegia was over 2 wks old but the K was 3.0 so is this an issue.

Just curious to see what others thought, noboby seemed to agree on anything and all just wanted to blame this incident on things that made them look the least bad.

she had underlying heart disease


I would argue against the succinylcholine as the culprit; she would not have come back with electricity.. She would have remained in v fib til something was done to promptly lower the K..


Sounds like a lot going on.. Need more info.. about how they diagnosed the Tb meningitis.. why does she have elevataed ICP necessitating a shunt? Is the TB in the lungs? is that whats causing the resp distress. Why cant this be preeclampsia ( severe) ? What did the head ct look like? Is the TB affecting the heart muscle causing a myocarditis affecting function of the heart? Lot of questions need answered.. What was all of the abg?

 

[militarymd]

meningitis can cause high ICP and hydrocephelus

 

[nitecap]

she had underlying heart disease


I would argue against the succinylcholine as the culprit; she would not have come back with electricity.. She would have remained in v fib til something was done to promptly lower the K..


Sounds like a lot going on.. Need more info.. about how they diagnosed the Tb meningitis.. why does she have elevataed ICP necessitating a shunt? Is the TB in the lungs? is that whats causing the resp distress. Why cant this be preeclampsia ( severe) ? What did the head ct look like? Is the TB affecting the heart muscle causing a myocarditis affecting function of the heart? Lot of questions need answered.. What was all of the abg?

Yes the meningitis had caused some inflammation of a ventricle in brain though not exact of which one. They were putting in the shunt to relieve the hydroceph and hopefully regain some lower ext motor function, sensory intact. There was no history of HTN, CAD though with the pg. guess she already had increased demand and workload. But at 29 yo was overall b/f this very healthy and active. From what I see she had no myocardial TB issues nor in lungs. The pulm infection was called RUL pneumonia and since then had cleared up after being on AB and intubated 2 days. Most were not wearing TB masks either.

ABG preop via radial stick 7.33, CO2 47, Po2 98, Sat 97,HCO3 27, Hgb 11, gluc 130.

 

[stephend7799]

From what I see she had no myocardial TB issues nor in lungs. .

How do you know?

 

[nitecap]

It was not in the chart, history, and no one including ID, OB, Neuro Surg, cardiology, that was consulted post V-fib, or anesthesia mentioned it, noted it, or discussed this after the fact. I suppose she could have, but regarding to what was known about this pt there was no TB effecting the heart.

 

[Noyac]

Hyperkalemia leads to prolonged P-R interval, prolongation of QRS interval, ST elevation, and peaked T-waves. The rhythm may degenerate into a sinusoidal pattern and ventricular tachycaria or fibrillation.

This pt has motor deficits and most definitely had a large increase in serum K. The IVC would be the delivery source of the K to the heart since it is coming from the lower extremities. The heart would recieve a very large conc. of K rich blood from the IVC which would cause it to possibly fibrillate. The conc would then be mixed with SVC blood, bringing the overall conc back towards normal. This is how I see it.

 

[jetproppilot]

Hyperkalemia leads to prolonged P-R interval, prolongation of QRS interval, ST elevation, and peaked T-waves. The rhythm may degenerate into a sinusoidal pattern and ventricular tachycaria or fibrillation.

This pt has motor deficits and most definitely had a large increase in serum K. The IVC would be the delivery source of the K to the heart since it is coming from the lower extremities. The heart would recieve a very large conc. of K rich blood from the IVC which would cause it to possibly fibrillate. The conc would then be mixed with SVC blood, bringing the overall conc back towards normal. This is how I see it.

I concur with your eloquent explanation, Noy.

If it looks like a duck, waddles like a duck, its a duck.

Post operative normal K doesnt rule out sux-induced hyperkalemia.

Additionally, how many times have you seen v-fib from induction-induced hypotension in the heart room? Pretty rare. Whats the chance of a 29 year old having v-fib from induction-induced hypotension? Really really really rare.

 

[Idiopathic]

Having seen sux-induced hyperkalemia way too often in older, sicker(?) patients, Ive never seen it present like this. I dont buy it. I do like Noyac's explanation, though. If it were able to be proven, it should be in JAMA.

Im more likely buying the fact that there is underlying disease not adequately explained/discovered with history. Id be interested to see what she really had in her CSF. Is this an AIDS/immunosuppressed patient?

 

[jetproppilot]

Cardio disagreeing saying moms heart is young and healthy and that he thinks should could have compensated well enough.

.

That kinda rules out the ischemia theory.

Young healthy hearts dont go into v fib unless theres a light socket with a fork in it that she was holding onto that youre not telling us about.

 

[militarymd]

I've seen a patient fib (young woman going for appy...kind of septic with hypotension) after induction....brought back quickly with electicity.


I've seen a patient arrest from hyperkalemia and sux...and resusictated that patient.

I've done lit searches and presented grand rounds on both patients.

This patient, although clincal history suggests hyperkalemia, just doesn't sound like hyperkalemia based on how easily she was resusicitated.

 

[Gator05]

I 'd have to agree that sux wasn't the best choice for this pt, UNLESS the airway was critical AND this was a crash c-section AND roc wasn't available AND local wasn't an option.

That said, the Bp wasn't wonderful to start with, and she was a bit tachy. Was there a component of lower spinal shock? A dry patient with spinal shock given a full induction does seem to be a setup for cardiovascular collapse.

Not that I've done a bunch of neuro either, but can't sux increase your ICP? In a patient who may already have an increased ICP?

Interesting case, thanks for posting.

 

[jetproppilot]

I've seen a patient fib (young woman going for appy...kind of septic with hypotension) after induction....brought back quickly with electicity.


I've seen a patient arrest from hyperkalemia and sux...and resusictated that patient.

I've done lit searches and presented grand rounds on both patients.

This patient, although clincal history suggests hyperkalemia, just doesn't sound like hyperkalemia based on how easily she was resusicitated.

It was a brand new defibrillator.

 

[nitecap]

I 'd have to agree that sux wasn't the best choice for this pt, UNLESS the airway was critical AND this was a crash c-section AND roc wasn't available AND local wasn't an option.

That said, the Bp wasn't wonderful to start with, and she was a bit tachy. Was there a component of lower spinal shock? A dry patient with spinal shock given a full induction does seem to be a setup for cardiovascular collapse.

Not that I've done a bunch of neuro either, but can't sux increase your ICP? In a patient who may already have an increased ICP?

Interesting case, thanks for posting.

As far as the spinal shock, Im not sure. Her lower ext paralysis occurs when the CSF build up and resultant hydrocephalus so In guessing it was prob a head issue not really a cord issue so sympathetic tone should be intact huh.

And Miller talks of Sux increasing ICP d/t fascicualtion but said if a agent that decreases ICP is given first than the increase that suxs would have cause should be reduced if non existant.