Scenario posed to me by ICU nurse

Lactic Acid? That's a new one for me.

Asystole that promptly was probably a vascular catastrophe of some sort. Let us not forget why he crashed the car (a PE? MI? CVA? Lost a bet?) as a source for his demise.
 
VentMedic said:
That was a big issue with MAST. It is still a concern for compression or entrapment.
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Right, but a high lactate doesn't tank the pH to the point that you arrest THAT quickly (if at all). Hell, usually it doesn't tank your pH for a good while after the initial insult. They'd get dyspneic, altered...and *maybe* arrest a few hours later from a pH less than 7. Seems sketchy.
 
I would also state some type of aortic injury. Tear maybe, the fact that he was asymptomatic to asystole im guessing against lactic acid cause and more towards traumatic aortic injury of some sort.
 
maxwell said:
Right, but a high lactate doesn't tank the pH to the point that you arrest THAT quickly (if at all). Hell, usually it doesn't tank your pH for a good while after the initial insult. They'd get dyspneic, altered...and *maybe* arrest a few hours later from a pH less than 7. Seems sketchy.
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Lactic acid is the result of tissue hypoxia and hypoperfusion which force cells to breakdown glucose anaerobically. When a large part of the body is compressed by the MAST or in some crush injury, anaerobic metabolism occurs. Considering the area of the lower extremities, that sudden change in pH when the blood with lactic acid is mixed into the central circulation can have profound results to the body quickly. As well, when the MAST was deflated, that was the equivalient to losing a significant volume of blood in a few seconds dramically affecting after load.
 
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These are more questions than suggestions:
Rhabdomylosis? Is it possible to have that without any outward signs of trauma or c/o pain? I have read that ODing on certain meds causes rhabdo.

Could it have been something similar to orthostatic intolerance/suspension trauma even though the patient was conscious?

What about an internal defibrillator that was dislodged during the crash? (Maybe I watch too much tv)

Is it possible to have some sort of pontine/midbrain injury that doesn't present with altered LOC or pain?

Doesn't your heart adjust its pump volume and/or rate when you are inverted? Could that sudden change cause an arrest?
 
I wonder if it's a combination of problems.

Possibly an aortic tear that pooled blood around the heart; all of the shunting from his lower extremities and abdomen provided enough blood for the 20 minutes he was upside down. Once he was right side up, the heart had nothing to pump, hypoexmia, maybe a few seconds of V-tach and then asystole.

Also, a cervical fracture that didn't severe the spinal cord until he was extricated. This possibly causing the apnea.

Crazier things have happened.
 
VentMedic said:
The most common fxs we see from rollovers, either in Trauma or SCI Rehab, are C1 -C2. The deficit may not be immediately apparent due to the ligaments holding the bones stable...until moved. Then, it may be death or the remainder of their life on a ventilator. However, if treated carefully, these two fxs can be the most stable and with a few months in a halo or C-collar, they may be just fine with minimal complications.

These fxs may also be hard to detect due to location which is why a CT Scan is used to clear rollover MVCs.

Neuro deficits are also not always obvious until the cord is damaged by bones fragments or swelling. I also don't always trust the patient to say "No, I don't remember losing consciousness". When you are dealing with C1-C2 damage, one would also have to consider the brainstem.
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Yep. You can also find C1 decapitation injuries as well.
ffemt8978 said:
Actually, I work under the protocols for the county in question, and I've posted our C-spine procedures on here before. We are not to use MOI as an indicator to initiate C-spine precautions...there's a list of criteria to be met first.

I'm wondering if the seat belt cause some Compartmentalization Syndrome.
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MOI is a very poor indicator of actual injury. It can suggest places to look for injury, but that's about it. As to the seatbelt causing a compartment syndrome... I highly doubt it. It takes a while for sufficient pressure to build within a closed compartment to shut down the vasculature.
ResTech said:
That's an interesting case to say the least. My thoughts are what other's have already said which is a spinal cord injury possibly and the manipulation from removing from the seatbelt was the final insult. With being suspended upside down in a vehicle by a seatbelt.... it is impossible to not have any manipulation of the c-spine no matter what technique you use.... KED board or not. Im not saying dont immobilize in that situation but thats an extremely hard position to immobilize someone... especially if its a heavier person.

Also, a first thought I had was an internal abd rupture or hemorrhage of some sorts that perhaps the lap belt was tamponading and upon release the pt. bled out. I know that's getting pretty creative but ne thing's possible, right? Or just from the blunt force the pt. had an aneurysm.

And the lactic acid possibility... I would have to say highly doubt it.... there would have to be a complete occlusion of blood flow to a particular region for an extended period of time (2-3hrs) before the anaerobic metabolism creates a level of lactic acid and potassium to cause death.

I would love to hear what the autopsy showed.
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CAOX3 said:
I would also state some type of aortic injury. Tear maybe, the fact that he was asymptomatic to asystole im guessing against lactic acid cause and more towards traumatic aortic injury of some sort.
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I'd think perhaps an aortic injury and perhaps a decap or C1-C2 injury that manifested itself upon extrication.
VentMedic said:
Lactic acid is the result of tissue hypoxia and hypoperfusion which force cells to breakdown glucose anaerobically. When a large part of the body is compressed by the MAST or in some crush injury, anaerobic metabolism occurs. Considering the area of the lower extremities, that sudden change in pH when the blood with lactic acid is mixed into the central circulation can have profound results to the body quickly. As well, when the MAST was deflated, that was the equivalient to losing a significant volume of blood in a few seconds dramically affecting after load.
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Lactic Acid production occurs any time the body has to break down glucose anaerobically. This can occur in compartment syndromes, crush injury, tourniquet application, and even during high output athletic activity. You won't normally see Lactic Acid levels during athletics that approaches anywhere near the levels you can see when blood flow stops in an area. LA buildup can be extremely uncomfortable...

IIRC, not can you get a pretty significant volume of low pH blood returning to central circulation, you also get a significant amount of potassium, myoglobin, and phosphorus (from rhabdomyolysis) from the injured area also returning to the central circulation.

Combine that with a C1-C2 injury and you've got a recipe for what happened...
 
I wanted to lean towards aortic injury (descending aorta tear?).
 
tom.watkins said:
So I was in the ICU today doing some rounds for class and an RN hit me up for my opinion on a call she heard about....
"A 50 y/o male patient was driving along the highway between Toppenish and Goldendale, (pretty desolate stretch of HWY 97 in Washington state) when he lost control of his vehicle for unknown reasons and drove off the road, rolling at least one time. Time to dispatch was apprx. 10 mins, and first medic unit on scene arrived about 20 mins later. Pt was upside down, secured by seatbelt and was unable to free himself. Reporting party was unsure about moving him so he left him in place untill medics arrived. EMT and medic "cleared" c-spine and noted that pt was A&O to person, place, time and event; also denies loss of conciousness, denies chest pain, denies SOB, CMS normal in upper extremeties. Apprx. 1 minute after cutting the pt loose and safely removing him from the vehicle he becomes apneic and pulseless. Fast patches placed on pt, monitor shows assystole in 3 leads; CPR and ACLS on scene and continued for 40 mins to the nearest hospital. Pt pronounced DOA by ER physician." So that's a brief synopsis of the call, and the RN wanted to know my ideas behind the pt's sudden downturn. She brought up the idea of a massive lactic acid release, which I guess is feesible, but I don't know what the pt's labs showed in regards to LA. I do know that he was negative for troponin, negative for thrombi and had a clean echo except for some minor mitral valve regurg. (although I'm not sure how the echo was done correctly since the pt never had a ROSC). I'm leaning towards a massive increase in preload following removal from the vehicle, possibly causing trauma to baroreceptors and subsequent drop in BP, although I don't know all the particulars about the pt, i.e. numbness in legs, pedal pulses, etc. Or maybe a transient thrombus? I'd appreciate any ideas you have.
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I would figure their could have been some internal bleeding. The man drove off the rd, flipped, and put yourself in this situation: Although their was a seatbelt worn, it doesn't prevent movement of the body entirely. The pt also could have been struck by random crap in his car (tossed around). On top of it all, the pt has arenaline running through his body from the mva. Therefore, not feeling pain (or much of) while beeing observed by onlookers at the scene. So you got internal bleeding, being tamponaded by the seatbelt for about 30 minutes......seatbelt is removed, and so the blood sitting still accumilated toxins.....how's that sound?
 
rescue99 said:
Orhtostatic Shock. There were no signs of trauma found, correct?
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umm...OrthO-static shock ;) C'mon all you Firefighters and mountain climbers! Suspension injury is the most plausible when no other cause could be determined. :)
 
This months issue of JEMS has a good article discussing this exact cause... Suspension Trauma.
 
would it be possible that while he was upside down 2 things could have happened, or one of these

1. he had a c-spine fx that, while upside down with no weight on his neck, didnt show since his torso was supported by his seatbelt

2. bleeding in his abd cavity that was partially controlled by his lapbelt until released, then allowing for a rapid deterioration

I would have boarded him regardless, any rollover has a high index of suspicion because of the various and unpredictable forces involved. (example: things flying around car, unknown number of flips, unknown angle of flip etc).

my policy, at least for those of less than 60 or so is that its better to board and them be ok, than to not and them hav a fx that i missed when clearing.
 
Lots of good dx's here! I'm gonna try and find out a little more about the case, and I'm definitely gonna check out that JEMS article on suspension injuries....side-note: i only need 2 tubes left to be done with medic school! Somebody do the EMS code dance for me and drum me up a couple of calls requiring my extensive intubation skills! Lol. But seriously, i need them....now. Tired of school....so very tired. :-)
 
tom.watkins said:
Lots of good dx's here! I'm gonna try and find out a little more about the case, and I'm definitely gonna check out that JEMS article on suspension injuries....side-note: i only need 2 tubes left to be done with medic school! Somebody do the EMS code dance for me and drum me up a couple of calls requiring my extensive intubation skills! Lol. But seriously, i need them....now. Tired of school....so very tired. :-)
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First - continuing good luck on school!

Second, suspension trauma is your most likely culprit. When you find the JEMS article, which is a pretty good one, you'll see the basic mechanism is the orthostatic intolerance of venous pooling in non-moving extremities leads to a significant amount of non-oxygenated blood just lying there until the patient is placed flat. Then bam! All that non-oxygenated blood hits the heart at once, the heart can't cope, and cardiac arrest is immediate. That's the theory in a nutshell.
 
So. IL Medic said:
First - continuing good luck on school!

Second, suspension trauma is your most likely culprit. When you find the JEMS article, which is a pretty good one, you'll see the basic mechanism is the orthostatic intolerance of venous pooling in non-moving extremities leads to a significant amount of non-oxygenated blood just lying there until the patient is placed flat. Then bam! All that non-oxygenated blood hits the heart at once, the heart can't cope, and cardiac arrest is immediate. That's the theory in a nutshell.
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This is a neat theory but even if you are suspended you still have a good blood pressure. Shouldn't have much venous pooling with proper heart function.
 
My first thought was an abd. aortic injury that caused his death when released from the seat belt. If there was a C1-C2 fx that very well could've caused death when released as well, maybe it was a combination of the two. Would be very interesting to see the coroner's report.
 
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