Good catch mate, pelvic wrap is a bloody fantastic idea.
We have gotten the commerical binders recently but used a sheet for years.
usalsfyre's Train Wreck #2
- Thread starter usalsfyre
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Good catch mate, pelvic wrap is a bloody fantastic idea.
We have gotten the commerical binders recently but used a sheet for years.
Seems a little sick.
A: Sounds like the surgical cric' was a good call. I might have tried a laryngoscopy just to see if I could pass an ET, but it's going to be difficult to adequately secure if the face is that fractured, and it sounds like RSI may take too long, as it's questionable whether we can get adequate BVM ventilation if the face is smashed, the airway's bloody, and the patient's already severely hypoxic.
Let's be sure that the cric' is correctly placed, and that we haven't managed to channel it through the trachea and into the esophagus. It sounds like we have CO2 and chest rise with ventilation through it.
B: SpO2 sucks. How's compliance? I'm guessing it sucks too. We have decreased A/E unilaterally, on the segmented side, and an angio dripping blood.
I know our JVD has gone since it's been placed, but did we hear air escape, did compliance improve? Has our JVD just diminished because we have no volume and no CVP? Did we actually have a tension / simple pneumo? Either case, I think we should attempt another decompression.
Need to suction the trachea. I'm thinking neurogenic pulmonary edema? Or a tracheal tear.
Should I trust the ETCO2, if the airways full of blood? How's the waveform look?
C: MAP is 74 mmHg. This isn't good.
D: Massive head trauma, multiple facial fractures, seizing / posturing, dilated poorly-reactive pupils, exopthalmus. Looks like he's herniating as well. He's missing the classic bradycardia, but perhaps this is a result of massive hypovolemia from the accompanying traumatic injuries.
Anything from the history to suggest possible illicit drug use? Complicating hypoglycemia seems staggeringly unlikely, but we should get a glucose as a r/o.
Other injuries: I think I agree with abckidsmom's suggestions. I guess he's not getting catheterised.
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Treatment plan:
Hyperventilate @ 20/min. Target ETCO2 is 30 mmHg.
The MAP is way too low. Aggressive fluid resuscitation to a MAP of >90 mmHg. So target systolic will probably be around 110-120 mmHg, if we assume ICP is around 25 mmHg (which is a big assumption). I'd throw in a 20ml/kg bolus as fast as humanly possible. Then I'm going to consider more fluids, with potential for a pressor.
Seizure might be due to herniation, might be due to hypoxia. Assuming this person is something around normal body weight, lets throw in 5mg midazolam IV.
[I recognise the potential for hypotension here. If we were just sedating, I'd consider ketamine, despite the debate about it's use in patients with elevated ICP. But we need an anticonvulsant here.]
I'm reluctant to paralyse here, because I'd like to know that I've controlled the seizure activity. So I'm going to hold off on that, and give the versed a few minutes to work. Then reassess my position.
[I recognise this is a huge judgment call. Seizing and paralysed is going to hugely increase metabolic demands on the brain. Not being paralysed is going to make this worse.]
I'd like to wrap the pelvis. Sheet and a couple of hemostats will work.
Not worried about the extremities, if the bleedings controlled. But we're going to have to re-assess that as we pressure infuse. If the patient becomes more stable, we can look at whether altering the alignment might improve peripheral vascular function.
Transport: Life threats here are herniation syndrome compressing the brainstem, and acute hemorrhage. His cranial vault needs decompressing, and someone needs to rearrange his internal organs. The Level II sounds good for now, as long as they can have someone there by the time the patient arrives.
If I can beat the chopper to the Level II, I'll transport. Otherwise they take them. Whatever gets him to a trauma surgeon quicker.
A: Sounds like the surgical cric' was a good call. I might have tried a laryngoscopy just to see if I could pass an ET, but it's going to be difficult to adequately secure if the face is that fractured, and it sounds like RSI may take too long, as it's questionable whether we can get adequate BVM ventilation if the face is smashed, the airway's bloody, and the patient's already severely hypoxic.
Let's be sure that the cric' is correctly placed, and that we haven't managed to channel it through the trachea and into the esophagus. It sounds like we have CO2 and chest rise with ventilation through it.
B: SpO2 sucks. How's compliance? I'm guessing it sucks too. We have decreased A/E unilaterally, on the segmented side, and an angio dripping blood.
I know our JVD has gone since it's been placed, but did we hear air escape, did compliance improve? Has our JVD just diminished because we have no volume and no CVP? Did we actually have a tension / simple pneumo? Either case, I think we should attempt another decompression.
Need to suction the trachea. I'm thinking neurogenic pulmonary edema? Or a tracheal tear.
Should I trust the ETCO2, if the airways full of blood? How's the waveform look?
C: MAP is 74 mmHg. This isn't good.
D: Massive head trauma, multiple facial fractures, seizing / posturing, dilated poorly-reactive pupils, exopthalmus. Looks like he's herniating as well. He's missing the classic bradycardia, but perhaps this is a result of massive hypovolemia from the accompanying traumatic injuries.
Anything from the history to suggest possible illicit drug use? Complicating hypoglycemia seems staggeringly unlikely, but we should get a glucose as a r/o.
Other injuries: I think I agree with abckidsmom's suggestions. I guess he's not getting catheterised.
---------------------------------------------------------------------
Treatment plan:
Hyperventilate @ 20/min. Target ETCO2 is 30 mmHg.
The MAP is way too low. Aggressive fluid resuscitation to a MAP of >90 mmHg. So target systolic will probably be around 110-120 mmHg, if we assume ICP is around 25 mmHg (which is a big assumption). I'd throw in a 20ml/kg bolus as fast as humanly possible. Then I'm going to consider more fluids, with potential for a pressor.
Seizure might be due to herniation, might be due to hypoxia. Assuming this person is something around normal body weight, lets throw in 5mg midazolam IV.
[I recognise the potential for hypotension here. If we were just sedating, I'd consider ketamine, despite the debate about it's use in patients with elevated ICP. But we need an anticonvulsant here.]
I'm reluctant to paralyse here, because I'd like to know that I've controlled the seizure activity. So I'm going to hold off on that, and give the versed a few minutes to work. Then reassess my position.
[I recognise this is a huge judgment call. Seizing and paralysed is going to hugely increase metabolic demands on the brain. Not being paralysed is going to make this worse.]
I'd like to wrap the pelvis. Sheet and a couple of hemostats will work.
Not worried about the extremities, if the bleedings controlled. But we're going to have to re-assess that as we pressure infuse. If the patient becomes more stable, we can look at whether altering the alignment might improve peripheral vascular function.
Transport: Life threats here are herniation syndrome compressing the brainstem, and acute hemorrhage. His cranial vault needs decompressing, and someone needs to rearrange his internal organs. The Level II sounds good for now, as long as they can have someone there by the time the patient arrives.
If I can beat the chopper to the Level II, I'll transport. Otherwise they take them. Whatever gets him to a trauma surgeon quicker.
fast65
Doogie Howser FP-C
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Well from the research I've been doing this morning, it seems as though the increased ICP stems from an impedance of cerebral venous return and a decrease of MAP, which influences CPP and could increase ICP. However, the studies I've found also stated that higher levels of PEEP (<30-40 mmH2O) could actually decrease ICP. Now, I'm sure that I've said something wrong here, so please, somebody smarter than me come correct me
Edit: Oh, and I completely forgot about the unstable pelvis, good catch pelagic.
So...
We put a pelvic binder on him and throw a three-way stopcock on the angio cath. There's a bit, not much sub-q air still noted. Waveform is present, but diminished. D stick is 106. A 250 ml bolus of fluid holds his pressure steady at least.
NVRob-is a tension hemo possible? Why or why not?
systemt-lorazepam might be a better seizure control medication in this case due to the hemodynamics, it tends to be a little stabler.
To the group-Why might his ETCO2 be so diminished? Is this necessarily reflective of his PaCO2? Are we going to paralyze him?
2mgs of lorazepam controls his seizure, but he's now totally out. Suctioning the tube out bumps his SpO2 into the mid 90s, but you can already see the beginings of the frothy stuff coming back.
Level II is a good choice. It has most of the capabilities of a level I, just generally on 15 minute call and not on campus.
Conclusion later on this evening or tommorow, and an explanation of what this call was based on.
We put a pelvic binder on him and throw a three-way stopcock on the angio cath. There's a bit, not much sub-q air still noted. Waveform is present, but diminished. D stick is 106. A 250 ml bolus of fluid holds his pressure steady at least.
NVRob-is a tension hemo possible? Why or why not?
systemt-lorazepam might be a better seizure control medication in this case due to the hemodynamics, it tends to be a little stabler.
To the group-Why might his ETCO2 be so diminished? Is this necessarily reflective of his PaCO2? Are we going to paralyze him?
2mgs of lorazepam controls his seizure, but he's now totally out. Suctioning the tube out bumps his SpO2 into the mid 90s, but you can already see the beginings of the frothy stuff coming back.
Level II is a good choice. It has most of the capabilities of a level I, just generally on 15 minute call and not on campus.
Conclusion later on this evening or tommorow, and an explanation of what this call was based on.
(1) Ativan vs. Versed -- I wasn't aware ativan was safer here. Looks like I have a little reading to do!
(2) Fluid resus: I've got to say again that it seems like we're under-resuscitating this patient.
We know that CPP = MAP - ICP. Right now, our MAP is only 74 mmHg. If the patient is showing signs of herniation, and brain stem dysfunction, we can probably assume that ICP is at least 25mmHg. It may be even higher. We can't know the exact value until the patient's receiving ICU care and has an ICP monitor on board.
So given these numbers we're looking at a CPP of 49 mmHg. This isn't enough to maintain cerebral perfusion. Most of the literature suggests a target CPP of around 65 - 70 mmHg, although this area is a little controversial. So we should be aiming for a MAP of at least 90. [We should also bear in mind that this may still be under-resuscitation, as the actual ICP may be much higher than 25mmHg]
Permissive hypotension is a well accepted treatment for adult multi-system trauma. I'm understand that aggressive crystalloid therapy is going to cause hemodilution, and that as we increase MAP our rate of internal hemorrhage is going to increase, and we risk popping thrombi. But if we don't adequately resuscitate the brain, we're just saving organs for donation (and the pickings here are slim!). Closed head injury is not the time for permissive hypotension.
Maybe something has changed and I'm out of date here?
(3) The relation between ETCO2 and PaCO2 is dependent upon the V/Q. If we have a low cardiac output state (as we have here), we may have many under-perfused lung units, which are being ventilated, but have minimal gas exchange occurring, and therefore minimal CO2 present. Upon exhalation, gas from these units is going to mix with gas from normally perfused and ventilated units, and effectively dilute the proportion of CO2. The loss of cardiac output from decreased CVP is probably also complicated by the effect of the neurogenic pulmonary edema on diffusion in the alveoli. And we have traumatic injuries that are impacting upon both ventilation and perfusion, in addition.
(4) Paralysis: If the patient's flat, and not fighting ventilation, I think I'll avoid it, so I can identify and treat further seizure activity.
(2) Fluid resus: I've got to say again that it seems like we're under-resuscitating this patient.
We know that CPP = MAP - ICP. Right now, our MAP is only 74 mmHg. If the patient is showing signs of herniation, and brain stem dysfunction, we can probably assume that ICP is at least 25mmHg. It may be even higher. We can't know the exact value until the patient's receiving ICU care and has an ICP monitor on board.
So given these numbers we're looking at a CPP of 49 mmHg. This isn't enough to maintain cerebral perfusion. Most of the literature suggests a target CPP of around 65 - 70 mmHg, although this area is a little controversial. So we should be aiming for a MAP of at least 90. [We should also bear in mind that this may still be under-resuscitation, as the actual ICP may be much higher than 25mmHg]
Permissive hypotension is a well accepted treatment for adult multi-system trauma. I'm understand that aggressive crystalloid therapy is going to cause hemodilution, and that as we increase MAP our rate of internal hemorrhage is going to increase, and we risk popping thrombi. But if we don't adequately resuscitate the brain, we're just saving organs for donation (and the pickings here are slim!). Closed head injury is not the time for permissive hypotension.
Maybe something has changed and I'm out of date here?
(3) The relation between ETCO2 and PaCO2 is dependent upon the V/Q. If we have a low cardiac output state (as we have here), we may have many under-perfused lung units, which are being ventilated, but have minimal gas exchange occurring, and therefore minimal CO2 present. Upon exhalation, gas from these units is going to mix with gas from normally perfused and ventilated units, and effectively dilute the proportion of CO2. The loss of cardiac output from decreased CVP is probably also complicated by the effect of the neurogenic pulmonary edema on diffusion in the alveoli. And we have traumatic injuries that are impacting upon both ventilation and perfusion, in addition.
(4) Paralysis: If the patient's flat, and not fighting ventilation, I think I'll avoid it, so I can identify and treat further seizure activity.
A couple of other thoughts:
(1) We have blunt chest injuries, and should do an ECG to see if we have conduction block / ST-T changes.
(2) We need to measure the patient's temperature, and protect against hypothermia.
(3) Can we do a FAST or iSTAT?
(4) We should give more consideration as to why the vehicle left the road. Of course, the patient being a poor driver has to be high on the index of suspicion. But do we have cointoxication with EtOH / other drugs?
(1) We have blunt chest injuries, and should do an ECG to see if we have conduction block / ST-T changes.
(2) We need to measure the patient's temperature, and protect against hypothermia.
(3) Can we do a FAST or iSTAT?
(4) We should give more consideration as to why the vehicle left the road. Of course, the patient being a poor driver has to be high on the index of suspicion. But do we have cointoxication with EtOH / other drugs?
Nope, quite simply, this guys jacked. Too much fluid will kill him, too low a MAP will kill him (or leave him ready to be planted in the cucumber patch).
In addition to the low output, remember he's got serious chest injuries, meaning the gas would have to diffuse through fluid as well. His PaCO2 is probably much higher than what is indicated by ETCO2.
Conclusion
So the patient is transported to the LII. Enroute he is suctioned frequently, appx 500mls of blood is suctioned from the ETT. He codes on arrival at the ED. After administration of blood products he has an ROSC, goes to surgery and lives through the inital surgery to repair the hemothorax. Pt has severe pulmonary contusions as well. Unfortunately an CT indicates little cereberal perfusion is present and and EEG is negative for brain activity. The patient fails multiple apnea test and is declared brain dead.
The patient is "based" off of a female passenger I responded to with that exact mechanisim of injury. She had a much more minor head injury but massive, massive chest injuries. The facial fractures were designed to get you thinking about situations where it is approprite to cric right off the bat.
Scenario #3 sometime next week, I've got another hellaciously busy week ahead.
So the patient is transported to the LII. Enroute he is suctioned frequently, appx 500mls of blood is suctioned from the ETT. He codes on arrival at the ED. After administration of blood products he has an ROSC, goes to surgery and lives through the inital surgery to repair the hemothorax. Pt has severe pulmonary contusions as well. Unfortunately an CT indicates little cereberal perfusion is present and and EEG is negative for brain activity. The patient fails multiple apnea test and is declared brain dead.
The patient is "based" off of a female passenger I responded to with that exact mechanisim of injury. She had a much more minor head injury but massive, massive chest injuries. The facial fractures were designed to get you thinking about situations where it is approprite to cric right off the bat.
Scenario #3 sometime next week, I've got another hellaciously busy week ahead.
abckidsmom
Dances with Patients
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This was a good one. I learned something new- that bit about the pulmonary hypoperfusion causing ETCO2 to be off. Worth it.
I once had a guy with similarly massive injuries, minus the head trauma. He lasted for 6 incredibly long hours once he got to our unit, 3-to-1 nursing staff and the trauma attending at the foot of the bed. It was a looooong, bloody shift.
fast65
Doogie Howser FP-C
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Wow usalsfyre, that was an amazing scenario, it really got me thinking, thanks! I look forward to your next scenario.
Sent from my mobile command center
Sent from my mobile command center
This was a great scenario. Thanks!
I agree that aggressive resuscitation is probably going to result in exsanguination. On the other hand, I know that underresuscitation with that sort of transport time is going to result in profound disability if the patient is herniating.
If the patient just has a simple head injury, or has a closed head injury wihout signs of herniation, then I'd be happy with a less aggressive approach with permissive hypotension.
Aidey
Community Leader Emeritus
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I believe that this guy is what is clinically known as "F*cked".
I'd have to do some research on this, but I'm going to hazard a guess that very few patients survive* a herniation that happens in the field. Increased ICP is a self perpetuating problem. The body compensates for the increased ICP by increasing the ICP, which in turn causes the body to increase the ICP. We can not stop this in the field. Decreasing the pts CO2 provides a minimal transient effect on ICP and will not stop someone from herniating.
Brutally and practically speaking this patient is going to die. You can either under resuscitate and possibly save his organs for donation** or you can flood him with saline in an attempt to achieve a higher MAP and hypoperfuse him into total organ failure. It is a crappy situation and there is no fixing this patient.
*Non eggplant survival.
** And/or give the family enough time to say goodbye.
I'd have to do some research on this, but I'm going to hazard a guess that very few patients survive* a herniation that happens in the field. Increased ICP is a self perpetuating problem. The body compensates for the increased ICP by increasing the ICP, which in turn causes the body to increase the ICP. We can not stop this in the field. Decreasing the pts CO2 provides a minimal transient effect on ICP and will not stop someone from herniating.
Brutally and practically speaking this patient is going to die. You can either under resuscitate and possibly save his organs for donation** or you can flood him with saline in an attempt to achieve a higher MAP and hypoperfuse him into total organ failure. It is a crappy situation and there is no fixing this patient.
*Non eggplant survival.
** And/or give the family enough time to say goodbye.
Aidey
Community Leader Emeritus
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I think it is the posturing and decreased LOC, but that is just a guess.
It's not something that I ever want to think about having to do, and would definetly be a time I'd be on the phone with the ER Doc (who'd probably be on the phone with an anesthesiologist who'd probably be on the phone with someone else) but this particular situation...might...maybe...be a time when using a pressor along with fluids could be beneficial to the patient. There is some info out there that has looked at using phenylephrine and vasopressin (not routinely carried I know) in hemmorhagic shock with concurrent TBI to maintain MAP's and CPP with better outcomes for the patient than just fluids.
No matter what you do, this guy is royally screwed, but, based on some info out there, using a pressor just might be somewhat beneficial...though probably only to the extent that he'd be a better organ donor.
Just more food for thought.
No matter what you do, this guy is royally screwed, but, based on some info out there, using a pressor just might be somewhat beneficial...though probably only to the extent that he'd be a better organ donor.
Just more food for thought.
Melclin
Forum Deputy Chief
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haemorrhagic shock + TBI = probable admission to the ECU.
Usal, stop posting these things when I'm at work. I can't keep up.
Its an interesting ballance, the fluid resus in TBI versus, hypotensive resus in haemorrhage. Do you pick one and hope for the best or do you hedge your bets and risk ending up in no mans land where you've effectively done neither.
My thoughts were to target a MAP or 80 based on what I've read in my trauma books.
Also the BTF have some nice little guidelines complete with evidence on this. They've been consistently revising down the necessary CPP for the past 5 years.
Currently a CPP > 50 is the go and they actually discourage aggressive attempts at getting it above 70. If we assume a ICP of 25 like you mentioned systemet, then we're talking a minimum MAP of 75, so a MAP of 80-85 seems good.
http://tbiguidelines.org/glHome.aspx?gl=1
I suppose it basically comes down to whose the bigger villein. The haemodilution or the hypotension. Off the top of my head, I'd guess hypotension. You can give a person PRBCs and FFP, but you can't give them back their brain. So maybe a higher target MAP might be a nice idea. I suppose it also depends on how much you have to infuse to achieve the target. If you gave 250mls and by pure magic the MAP hit 80, maybe you might think about more. If it took a 1500mls, maybe you leave it there. Just thinking out loud. What do we think?
Usal, stop posting these things when I'm at work. I can't keep up.
Its an interesting ballance, the fluid resus in TBI versus, hypotensive resus in haemorrhage. Do you pick one and hope for the best or do you hedge your bets and risk ending up in no mans land where you've effectively done neither.
My thoughts were to target a MAP or 80 based on what I've read in my trauma books.
Also the BTF have some nice little guidelines complete with evidence on this. They've been consistently revising down the necessary CPP for the past 5 years.
Currently a CPP > 50 is the go and they actually discourage aggressive attempts at getting it above 70. If we assume a ICP of 25 like you mentioned systemet, then we're talking a minimum MAP of 75, so a MAP of 80-85 seems good.
http://tbiguidelines.org/glHome.aspx?gl=1
I suppose it basically comes down to whose the bigger villein. The haemodilution or the hypotension. Off the top of my head, I'd guess hypotension. You can give a person PRBCs and FFP, but you can't give them back their brain. So maybe a higher target MAP might be a nice idea. I suppose it also depends on how much you have to infuse to achieve the target. If you gave 250mls and by pure magic the MAP hit 80, maybe you might think about more. If it took a 1500mls, maybe you leave it there. Just thinking out loud. What do we think?