Shotgun - Pregnant female scenario

[JeffDHMC]

I'm not so sure about a 12 lead either, but I would hook her up to a 3 lead with the combo pads just incase she de-compensates.

Not going to help lad. Needs a surgeon.

 

[jrbigelow]

Make sure you get a couple of large bore IVs. Your big problem is going to be hypovolemic shock. Might be a good idea to review your drip rates for dopamine.

Please tell me you are joking about the dopamine for hemoragic shock? Correct me if I'm wrong, and well, I know I'm not, but you don't give dopamine for hemoragic shock. You might want to recheck your medication contraindications, not to mention common sense.

 

[kittaypie]

Not going to help lad. Needs a surgeon.

yes she needs a surgeon but what are you going to do if she codes on the gurney with no leads or pads on? scramble to get everything ready instead of preparing for it?

 

[Jeffrey_169]

I am more experienced as a Basic then a Medic (as I have only been a medic a few months), but why would you defib. a trauma pt? The H's and T's are your issue, and until they are properly addressed defibrillating will only damage the heart further, right?

 

[kittaypie]

I am more experienced as a Basic then a Medic (as I have only been a medic a few months), but why would you defib. a trauma pt? The H's and T's are your issue, and until they are properly addressed defibrillating will only damage the heart further, right?

if a trauma patient is bad enough to be in cardiac arrest, the last thing I'm going to worry about is a little electrical damage to the heart. basically the only thing we can do for this patient is aggressive fluid resuscitation and proper oxygenation. if, despite all this, she arrests and goes into vfib/vtach,
I wouldn't skip a beat (no pun intended) in defib-ing. at that point, it's their only chance of survival.

 

[Jeffrey_169]

I see your point. We're taught a little bit differently. In the trauma situation we were taught to treat the cause because defib. won't help until you treat the underlying cause(s). I think its a matter of protocol and state requirments. They taught we could apply it if we had time, but not to make it a prioty. Another reason could be becasue we have paddles here, and we were taught the "quick look method" where the patches are not necessary; we can use the paddles to get a picture of the rhythm.
Regardless, I do see your point. "Treat the pt. not the text book"

 

[kittaypie]

I'm confused about your treatment. if you saw a shockable rhythm on the monitor would you just continue with fluids? I see your point in treating the underlying cause, but if the patient is not perfusing wouldn't you rather shock and possibly get a rhythm back (thus aiding perfusion) or just leave them in the rhythm and continue other treatments?

 

[Lifeguards For Life]

Please tell me you are joking about the dopamine for hemoragic shock? Correct me if I'm wrong, and well, I know I'm not, but you don't give dopamine for hemoragic shock. You might want to recheck your medication contraindications, not to mention common sense.

Dopamine is indicated in situations where we need to increase end-organ perfusion in patients in cardiogenic shock, or in hemodynamicaly significant hypotension. A relative contraindication is hypovolemia in cases where complete fluid resuscitation has not been attempted.

Dopamine is a dose dependant drug, meaning there is a different mechanism of action at different dosages. At low dosages (1 to 5mcg/kg/minute), dopamine directly stimulates dopaminergic receptors on arteries in the kidneys, abdomen, heart, and brain and causes vasodilatation. At these doses, urine output may increase, but blood pressure and heart rate are usually not affected.

Correct me if I'm wrong, and well, I know I'm not, but Dopamine in low dosages would be a"very bad thing"

The leading cause of death with regard to civilian and military traumas is hemorrhagic shock.1 Since hemorrhagic shock has a high mortality rate, research is crucial in finding the most effective treatment. The article provides a review of the 4 types of shock, the 4 classes of hemorrhagic shock, and the latest research on resuscitative fluid. The 4 types of shock are categorized into distributive, obstructive, cardiogenic, and hemorrhagic shock. Hemorrhagic shock has been categorized into 4 classes, and based on these classes, appropriate treatment can be planned. Crystalloids, colloids, dopamine, and blood products are all considered resuscitative fluid treatment options. Each individual case requires various resuscitative actions with different fluids. Healthcare professionals who are knowledgeable of the information in this review would be better prepared for patients who are admitted with hemorrhagic shock, thus providing optimal care.

Correct me if I'm wrong, and well, I know I'm not, but at higher dosages (greater than 10 mcg/kg/min), Dopamine exerts effects primarily alpha-receptors, and extensive vasoconstriction causes blood pressure to increase.

http://www.ncbi.nlm.nih.gov/pubmed/8124958
http://www.abbott.com.pk/pdf/DOPAMINEPI.PDF
http://www.nursingcenter.com/prodev/ce_article.asp?tid=774877
http://www.koreamed.org/SearchBasic.php?DT=1&RID=174302

While I would not be pushing Dobutamine at the point in time described by the original poster, you may wish to reconsider your statements regarding the use of Dobutamine and hemorrhagic shock

"You might want to recheck your medication contraindications, not to mention common sense."

 

[Jeffrey_169]

In this case I would treat for shock, high flow O2, and bleeding control. I would most likely apply the three lead so I could maintain a visual on what the heart is doing, but the shock would be my main concern. I do not want her gong into shock. My job here is to prevent the patient from going into V-Tac/ V-fib. In this scenario the patient is slightly hypotensive and presents with a severe bleed, so these are my first concerns.

IN this scenerio she is conscious, has a pulse, is slightly hypotensive, RR are rapid, adn obviously has a pulse. My priority is to prevent her from getting worse, going into shock, and disrhythmias.

Again I am saying you are wrong, and I am not saying I completely disagree with you. I just think there are drugs which can do more, and taking time to set up a 12 lead would not be high on my list in this case. I could be wrong, as stated above, and the truth is you probably have more experience then I as a Paramedic, but this is simply my opinion.

 

[Lifeguards For Life]

In this case I would treat for shock, high flow O2, and bleeding control. I would most likely apply the three lead so I could maintain a visual on what the heart is doing, but the shock would be my main concern. I do not want her gong into shock. My job here is to prevent the patient from going into V-Tac/ V-fib. In this scenario the patient is slightly hypotensive and presents with a severe bleed, so these are my first concerns.

IN this scenerio she is conscious, has a pulse, is slightly hypotensive, RR are rapid, adn obviously has a pulse. My priority is to prevent her from getting worse, going into shock, and disrhythmias.

Again I am saying you are wrong, and I am not saying I completely disagree with you. I just think there are drugs which can do more, and taking time to set up a 12 lead would not be high on my list in this case. I could be wrong, as stated above, and the truth is you probably have more experience then I as a Paramedic, but this is simply my opinion.

I am not in disagreeing with you. As stated, regarding this patinets vitals and mechanism of injury, my treatment plan would mainly be supportive, while anticipating how this patient will be presenting in the next few seconds. At the point in time described by the OP I would not be pushing Dopamine, I only disagree with the jbigelows incorrect blanket statement and insulting demeanor.

It has just now came to my attention that this post was probably not directed toward me, but Kittaypie......

oh well

 

[redcrossemt]

I see your point. We're taught a little bit differently. In the trauma situation we were taught to treat the cause because defib. won't help until you treat the underlying cause(s). I think its a matter of protocol and state requirments. They taught we could apply it if we had time, but not to make it a prioty. Another reason could be becasue we have paddles here, and we were taught the "quick look method" where the patches are not necessary; we can use the paddles to get a picture of the rhythm.
Regardless, I do see your point. "Treat the pt. not the text book"

Applying defib patches isn't a bad idea, but I'd probably be so busy with other stuff that I probably and unfortunately wouldn't get to them until the patient coded.

Defibrillation in traumatic arrests... interesting stuff. I guess I would attempt defibrillation while continuing aggressive fluid management. Probably won't do much good unless you can fix the H's and T's, but at the same time, fluid resuscitation is not going to magically convert v-fib to a perfusing rhythm.

Research shows patches have significantly faster times to shock delivery, and they free up your hands... Many services and hospitals no longer have external paddles, which is a good thing.

12-lead is useless here. No one's advocating that.

 

[Smash]

I'm confused.

Can I get a quick straw poll here: How many people actually advocate cyclic crystalloid resuscitation (aggressive fluid administration) for an uncontrolled, penetrating truncal trauma? Hands up high so I can count them!

Ok, now who advocates the use of either "renal dose" dopamine or pressors in said uncontrolled penetrating truncal trauma? Hands up! Higher, don't be scared!



Let me tally the votes and I'll get back to you with your marks.

 

[Veneficus]

Ok, now who advocates the use of either "renal dose" dopamine or pressors in said uncontrolled penetrating truncal trauma? Hands up! Higher, don't be scared!.

I advocate unequivically not to put crystalloid in any uncontrolled bleeding.

please see my earlier comments.

it is the truncal trauma that I would say rules out the dopamine as it will actually dilate central artioles through D1 and D2 receptors. That would likely increase the rate of bleed as well as "tank" expansion.

My adding caveats probably doesnt help the pole.

 

[Smash]

On the contrary, it shows a good appreciation of the physiology, pathophysiology and aims of treatment that we are after.

Ok, I'll just come out and say it. In the setting of uncontrolled hemorrhage in the prehospital setting there is absolutely no role for dopamine, or any other inotropes. There is a role for such agents after the damage control surgery has been carried out to maintain perfusion. You need to plug the hole first though.

There are some major issues with using either "renal dose" dopamine or higher doses:

"Renal dose" dopamine (as venficus pointed out) dilates your afferent renal arterioles. This is then thought to improve renal blood flow, which we want to maintain - if your kidneys die, you die. However, for this to be effective, you need something to flow through them in the first place. Which the hemorrhaging shocked patient doesn't have. All that is going to happen is that you are going to increase the intravascular volume that needs to be filled with the precious little red stuff that remains. Furthermore, whilst studies have shown that low does dopamine improves O2 tensions in the kidneys and liver, it decreases flow to the gut. This causes all sorts of ongoing problems assuming that the patient survives: the gut is very, very important, far more so than we usually give it credit for being.

Ultimately, despite many studies into renal dosing of dopamine in many critically ill patients of varying etiologies, there is extremely scant evidence that there is any increase in survival despite the improvement in physiological parameters.


There is also no role for higher doses of dopamine or any other vasoactive drugs in the setting of uncontrolled hemrrhage. These patients are already maximally vasoconstricted: no further benefit can be gained in attempting to vasoconstrict further, and all of these drugs (dopamine, dobutamine, epi, nor-epi) cause profound myocardial hypoxia and dysfunction and are extremely arrythmogenic in this setting.

Aggressive fluid resuscitation is also an absolute no-no in uncontrolled hemorrhage. Whilst the finer points of how/when/where/why and how much are still being worked on, I know of no reputable trauma surgeon who would advocate the old formula of 3:1 fluid resuscitation for uncontrolled hemorrhage in the prehospital setting. Heck, in my service that would get me fired!

Karim Brohl (owner of Trauma.org, surgeon and contemporary of Ken Mattox) states: ALS/ACLS algorithms DO NOT APPLY to traumatic arrest.

The primary causes of traumatic arrest are hypoxia, hypovolaemia due to haemorrhage, tension pneumothorax, and cardiac tamponade. Hypoxic arrests respond rapidly to intubation and ventilation. Hypovolaemia, tension pneumothorax and cardiac tamponade are all characterised by loss of venous return to the heart. External chest compressions can provide a maximum of 30% of cardiac output in the medical arrest situations and are dependent on venous return to the heart. Chest compressions in the trauma patient are wholly ineffective, may increase cardiac trauma by causing blunt myocardial injury and obstruct access for performing definitive manoeuvers.


The treatment of massive thoracic haemorrhage is control of haemorrhage, not intravenous fluid therapy. Fluid therapy prior to haemorrhage control worsens outcome in penetrating thoracic trauma (and perhaps all penetrating trauma patients). If there is no response to a small (500ml) fluid challenge, fluid administration should be halted until haemorrhage control is achieved.

This is obviously problematic if the patient arrests in the field with no means of controlling the bleed. Actually, maybe it isn't problematic: if this happens, the patient is dead.

VF/VT are unlikely to be your presenting rhythms in arrest following exsanguination, and it is highly unlikely that defib is going to be of any benefit in this scenario anyway.

 

[pvfd62med22]

i agree and think that your time would be much better spent doing a host of other services to this patient than getting a EKG

In MA at my service that's what us basics are for We hook up the 12 leads and stuff while the medic does his interventions.. And since we r in the sticks up here.. we would draft a cop or FF to drive and we would both be in back:wacko:..

 

[Veneficus]

On the contrary, it shows a good appreciation of the physiology, pathophysiology and aims of treatment that we are after.

Ok, I'll just come out and say it. In the setting of uncontrolled hemorrhage in the prehospital setting there is absolutely no role for dopamine, or any other inotropes. There is a role for such agents after the damage control surgery has been carried out to maintain perfusion. You need to plug the hole first though.

There are some major issues with using either "renal dose" dopamine or higher doses:

"Renal dose" dopamine (as venficus pointed out) dilates your afferent renal arterioles. This is then thought to improve renal blood flow, which we want to maintain - if your kidneys die, you die. However, for this to be effective, you need something to flow through them in the first place. Which the hemorrhaging shocked patient doesn't have. All that is going to happen is that you are going to increase the intravascular volume that needs to be filled with the precious little red stuff that remains. Furthermore, whilst studies have shown that low does dopamine improves O2 tensions in the kidneys and liver, it decreases flow to the gut. This causes all sorts of ongoing problems assuming that the patient survives: the gut is very, very important, far more so than we usually give it credit for being.

Ultimately, despite many studies into renal dosing of dopamine in many critically ill patients of varying etiologies, there is extremely scant evidence that there is any increase in survival despite the improvement in physiological parameters.


There is also no role for higher doses of dopamine or any other vasoactive drugs in the setting of uncontrolled hemrrhage. These patients are already maximally vasoconstricted: no further benefit can be gained in attempting to vasoconstrict further, and all of these drugs (dopamine, dobutamine, epi, nor-epi) cause profound myocardial hypoxia and dysfunction and are extremely arrythmogenic in this setting.

Aggressive fluid resuscitation is also an absolute no-no in uncontrolled hemorrhage. Whilst the finer points of how/when/where/why and how much are still being worked on, I know of no reputable trauma surgeon who would advocate the old formula of 3:1 fluid resuscitation for uncontrolled hemorrhage in the prehospital setting. Heck, in my service that would get me fired!

Karim Brohl (owner of Trauma.org, surgeon and contemporary of Ken Mattox) states: ALS/ACLS algorithms DO NOT APPLY to traumatic arrest.

The primary causes of traumatic arrest are hypoxia, hypovolaemia due to haemorrhage, tension pneumothorax, and cardiac tamponade. Hypoxic arrests respond rapidly to intubation and ventilation. Hypovolaemia, tension pneumothorax and cardiac tamponade are all characterised by loss of venous return to the heart. External chest compressions can provide a maximum of 30% of cardiac output in the medical arrest situations and are dependent on venous return to the heart. Chest compressions in the trauma patient are wholly ineffective, may increase cardiac trauma by causing blunt myocardial injury and obstruct access for performing definitive manoeuvers.


The treatment of massive thoracic haemorrhage is control of haemorrhage, not intravenous fluid therapy. Fluid therapy prior to haemorrhage control worsens outcome in penetrating thoracic trauma (and perhaps all penetrating trauma patients). If there is no response to a small (500ml) fluid challenge, fluid administration should be halted until haemorrhage control is achieved.

This is obviously problematic if the patient arrests in the field with no means of controlling the bleed. Actually, maybe it isn't problematic: if this happens, the patient is dead.

VF/VT are unlikely to be your presenting rhythms in arrest following exsanguination, and it is highly unlikely that defib is going to be of any benefit in this scenario anyway.

I have had the honor of Meeting Dr. Brohi in person as well as spending several days with his service.

Like most contemporary trauma surgeons, 1:1:1 blood products as demonstrated abundantly in recent wars is the goal of fluid replacement. Some of the contemporaries also advocate 3:3:1 or other massive transfusions.

I wasn't advocating dopamine as a method to help maintain renal perfusion with a bleed, I was suggesting it could be used to help control peripheral bleeding, by its mechanism. Also epi can be used topically to help localize and control bleeding. While often used in surgery, it can be used in the ED (A&E) as well. I can't think of any reason it could not be applied prehospital for the same.

Like any other tool in the box, vasoconstrictors have a time and place, I agree with an uncontrolled bleed it is not the time or place. As well, if you are using ACLS arrest procedures, the outcome will be an extremely stable patient. Delta G will = 0, doesn't get any more stable than that

 

[PrincessAnika]

just out of curiousity (coming from a basic/exmedic student - long story) - exactly how big is this hole? we are not qualified nor cleared to do emerg. c/s in the field but what would be the ruling, if the hole is big enough to pull baby out of?

 

[Smooth]

i've heard of a shotgun wedding but a shotgun pregnancy!

 

[terrible one]

Wow interesting read ... and I didn't get through them all,
12 Leads? RSI? Dopamine?

What else do we carry in the bus that will be time consuming and ineffective?
Thisn pt needs a surgeon asap, O2, control bleeding, grab some lines while en-route. I dont know why we are doing much of anything else, maybe i just missed something...?