Interesting, tragic case

[MP18D]

Had an interesting case today.

Pt is a 15y/o male.
"Buddies" have him in the back seat of their vehicle looking for a fire station.
He is pulseless/apneic. Fire is doing CPR when you arrive.
"Buddies" state they don't know what happened. They were all horseing around when their friend just fell out.....
While doing your Primary survey, you see a small, 1cm bruise center-mass on the chest. Otherwise unremarkable!
Medical history is unknown, but "buddies" tell of no medical problems they know of, just before they split...........

Dx?
Tx?

[http://home.mdconsult.com/das/journal/view/29936943/N/11985811?sid=194121773&source=MI

The significance to SF types is that operators can sustain blunt chest trauma through any number of mechanisms either during PT, training or Ops and Commodio should certainly be considered, even though the prognosis is poor.

[shadowflyer]

After researching since I have no real training...(not yet..;) ) ABC's would be the first thing. Continue with CPR and go from there. I did find a good page on Blunt Chest Trauma in which the method of injury was similar to this case.

Blunt Chest Trauma (http://www.kumc.edu/SAH/resp_care/thorcour.html)

[RIT_MEDIC]

Dx--cardiac arrest, origin unknown. Cardiac Tamponade??

Tx:
1.) Quick look w/ LP-12
Depending on rhythm follow ACLS protocol(s) ie: drugs and defib/ pacing.

2.) Intubate..check lung sounds thoroughly(not that you would not any other time) possible pneumo/hemothorax.

3.) IV 18ga NS

4.) Check BGL and Core temp

5.) Move to Bus

6.) High flow ambulance

7.) Question friends to find out what events they were participating in today just before pt collapsed and actual down time.

Reassess enroute to ER and change Tx accordingly.

[Axe]

Long QT interval comes to my mind first.

[Sneaky SF Dude]

1) ABCs
2) Check for Beck's Triad - falling blood pressure, rising jugular venous pressure, muffled heart sounds with the last being the least reliable sign of the three. If present, take appropriate action.
3) I would be very careful of fluids
4) I wouldn't have access to check rythms or an AED.

[TacMedic105]

Commotio Cordis (not sure on spelling) possibly? I had a 9y/o male die due to a line drive to the chest while playing baseball a few years ago. A diagnostic pericardiocentesis would either r/o or r/i tamponade.

Anyways-

ABC's
Quick-Look
Defib 200j/300j/360j if VF/VT
CPR
ETT/IV
Meds appropriate for rhythm
Diagnostic treatments (chest decompression prn, pericardiocentesis, Narcan, NaHCO3.

Any further info?

Andy

[mac3982]

why narcan? just askin ..protocol.. maybe ...blunt trama acls.. air way quick look....cpr iv..ips....jvd hemopeumo.. the protocals in the field in my area are regional...in one area they are aggresive in the city its blows load and give a right foot bolus.....bein a kid go all out....muffed heart tones...?treat per protocal.......

[Doc T]

Originally posted by Sneaky SF Dude
1) ABCs
2) Check for Beck's Triad - falling blood pressure, rising jugular venous pressure, muffled heart sounds with the last being the least reliable sign of the three. If present, take appropriate action.
3) I would be very careful of fluids
4) I wouldn't have access to check rythms or an AED.

so assume you notice the JVD and the child is in arrest...what would you do next? why careful with fluids?

[MP18D]

OUTSTANDING!!
You all rock! Obviously a bunch of knowledge and experience here. Thanks to USSFPA for kicking this whole idea off!

This is kinda tricky in the field; no one knows nothing, or is sayin nothin. So do you go down the medical path, push drugs, ACLS x a bunch, well into sodium bicarb?? Or do you treat as trauma and move out??

Old geezers(like me) are easy. We assume medical. Younger folks are different. Drug OD (Narcan-good idea) Congenital cardiac (Prolonged QT-another good thought) Fight, penetrating trauma????
Try and start lines, or just go...the questions can go on forever. And all the Docs I have worked with have their own thoughts. Not sure if there is a right or wrong answer past the basics; ABCs, quick ALS interventions and transport. DocT?

Anyhow I first saw a Commotio cordis (Good job TacMedic)in 97 or 8 at the ER I worked. Kid was playing 3rd base, took a bad hop to the chest and went down. Medics transported him, we tried synchronized cardioversion for his mixed idioventricular/SVT/V-tach/NSR bag for a long time in the ED. Cardiologist came down but didnt have much to add. He made it to the ICU and overnite just converted. Walked out a day later!!

When I get to work tomorrow I will try n figure out how to cut/paste that article off of Medline (Sorry Rsov) to the forum. It's about 3 pages; talks of early fears of tamponade (which is where the whole "blunt trauma with body armor" worries first came from: unfounded) and other ideas.

Research now shows that a small amount of force (kick, punch etc) at just the right time in the repolarization phase of the cardiac muscle can result in sudden death. Survivability is like 7%. Kinda like my marriages....
The articles all say that early and often electricity is key!

This type of syndrome was also looked into when flash-bangs (OK, distraction devices) first came into the civilian HRT arena. The worry there was overpressure in a confined space. Unfounded. There are a bunch of other references also. It is easy to see the relation to our work in the field/BAS etc.

The rest of this story is: Medics, who are some of the best in our area, did pretty much what you all said; ABCs, quick look, ACLSx1 and transport. They briefly got a bit of a perfusing V-Tach/Fib, but that was gone when they hit our door.

While the rest of the crew did their thing, I took a look with the bedside ultra-sound, confirmed it with the ED physician as no cardiac activity. The medic report was "unknown but prolonged down time in the field with at least 5-7 mins of CPR before ALS arrival". He was already a bit mottled. We called it.

A further survey revealed right scrotal swelling and bruising. When the S.O. found one of his homies, something was said about a fight. "But I did'nt see nuthin"

I was 0/5 yesterday. Oh well.

Once again, nice work folks.

[mac3982]

the lack of o2 and the prolonged down time....with emd would acidous be a factor in this case as well?.....

[frogstyle]

MP18D,
Thanks for sharing. This is good stuff. And we can all learn more.

B

[RIT_MEDIC]

How easy we forget the things we seldom, if ever see.


so assume you notice the JVD and the child is in arrest...what would you do next...

Pericardiocentesis??

Lots of good information being passed here.

Thanks USSFPA for the Forum and thanks MP18D for the case study.

James D.

[Sneaky SF Dude]

right Pericardiocentesis

I want to be careful of the fluids because 1) He's not losing any, so no need to pump him full. 2) I would think that fluid bolus could result in further complications with the pericardial tamponade.

[TacMedic105]

Originally posted by mac3982
the lack of o2 and the prolonged down time....with emd would acidous be a factor in this case as well?.....

Acidosis in cardiac arrest is most often respiratory in nature, as opposed to metabolic. For this reason, hyperventilation is the preferred method of treating an arrest-related acidosis, unless a stat ABG shows a metabolic acidosis. In this case, NaHCO3 would be indicated. If there is no access to an ABG, NaHCO3 should not be given unless the patient has been intubated and adequately ventilated for a good period of time. Hope this helps.

Andy

[TacMedic105]

Originally posted by Sneaky SF Dude
right Pericardiocentesis

I want to be careful of the fluids because 1) He's not losing any, so no need to pump him full. 2) I would think that fluid bolus could result in further complications with the pericardial tamponade.

Sneaky-

I seem to remember reading somewhere that patients with a significant tamponade can become hypovolemic due to the amount of blood that is pooled in the pericardial sac being significant, and that volume is not participating in perfusion. But I may be wrong.

I probably wouldn't get VERY aggressive with fluids until I had either ruled out or corrected the tampondae via a pericardiocentesis.

Andy

[themadmedic]

Initially, the fluid bolus can increase preload, helping to overcome the increased cardiac resistance from the tamponade, allowing for some perfusion. Of course, this can't last forever...

[Doc T]

[i]
I seem to remember reading somewhere that patients with a significant tamponade can become hypovolemic due to the amount of blood that is pooled in the pericardial sac being significant, and that volume is not participating in perfusion. But I may be wrong.

Andy [/B]

tamponade in and of itself does not allow for enough blood loss to cause hypovolemic shock...the pericardium just won't stretch enough to hold that much blood. Now, if there is a hole in the pericardium that leaks intermittently into the chest cavity then that is another story all together.

the reason you see hypotension with a tamponade is because the pressure builds up in the pericardial sac and doesn't allow the heart to contract and distend normally leading to a very low cardiac output.

Volume challenges are actually recommended because augmenting the fluid going into the heart (preload) can actually cause it to fill better despite the increased external pressures {as already mentioned earlier as increasing preload}...so aggressive fluid management would be indicated both before and after pericardiocentesis in an effort to maintain a blood pressure/cardiac output.

doc t.

[MP18D]

I will try to attach the journal article.....


American Journal of Emergency Medicine
Volume 19 • Number 5 • September 2001
Copyright © 2001 W. B. Saunders Company





Brief Reports

--------------------------------------------------------------------------------


Commodio cordis: An underappreciated cause of sudden cardiac death in young patients: Assessment and management in the ED




Andrew D. Perron MD
William J. Brady MD
Brian F. Erling MD


Key words
Commodio cordis


cardiac concussion


sudden cardiac death


sports injuries




--------------------------------------------------------------------------------
From the Department of Emergency Medicine, University of Virginia Health System, and the Department of Emergency Medicine, University of Virginia, Charlottesville, VA.
Manuscript received February 8, 2001.
Accepted February 28, 2001.

--------------------------------------------------------------------------------
Address reprint requests to Andrew D. Perron, MD, Assistant Professor of Emergency Medicine and Orthopedic Surgery, Department of Emergency Medicine, Box 800699, University of Virginia Health System, Charlottesville, VA 22908. E-Mail: adp9b@virginia.edu

Copyright © 2001 by W.B. Saunders Company



0735-6757/01/1905-0005$35.00/0





Commotio cordis is the condition of sudden cardiac death or near sudden cardiac death after blunt, low-impact chest wall trauma in the absence of structural cardiac abnormality. Ventricular fibrillation is the most commonly reported induced arrhythmia in commotio cordis. Blunt impact injury to the chest with a baseball is the most common mechanism. Survival rates for commotio cordis are low, even with prompt CPR and defibrillation. (Am J Emerg Med 2001;19:406-409. Copyright © 2001 by W.B. Saunders Company)




Commotio cordis was first named and systematically described in 1932, although there are earlier references to its existence.[1] [2] Commotio cordis (or cardiac concussion) refers to blunt, nonpenetrating, precordial chest injury that causes a malignant cardiac arrhythmia and sudden death. In most instances, the injury to the chest wall is relatively minor, and on autopsy there is no evidence of structural cardiac abnormality or induced cardiac injury. This absence of morphologic cardiac injury is what distinguishes commotio cordis (concussion) from contusio cordis (cardiac contusion with evidence of structural damage).[3] Commotio cordis occurs most frequently in young children, with the highest reported incidence in baseball, softball, and ice hockey.[3] [5] Other sports where commotio cordis have been reported include football, boxing, lacrosse, cricket, basketball, and martial arts.[3] [5] [6] Cases associated with nonsports scenarios have been reported from motor vehicle crashes, fights, and 2 cases of child abuse.[5] [7] [9]

Survival after commotio cordis has been reported, but is rare.[3] [4] [6] [10] Death is thought to result from primary ventricular fibrillation.[3] [4] The most common proposed mechanism for commotio cordis is believed to involve chest wall trauma that coincides with the vulnerable period of cardiac repolarization (T-wave).[3] [4] [8] [11] Other mechanisms that have been postulated but not proven include coronary artery vasospasm, asystole, hypervagatonia, and the long QT syndrome.[12] [15]

Epidemiology
The true incidence of commotio cordis is unknown. It is thought that commotio cordis goes underreported because it is often unrecognized. As of July 1, 1998, there were 70 individual case reports of commotio cordis reported in the literature and tabulated in the United States Commotio Cordis Registry (Minneapolis, MN). The mean age of victims in the registry is 12 years, with a range of 2 to 38 years. Of the patients, 70% are younger than 16 years. Sixty-nine of 70 (98.6%) of patients are males, and 61 of 70 (85.7%) are Caucasian. Approximately 50% of victims were participating in organized athletic activity, and 50% were outside organized sports.[6]

Most victims are seen to suffer a direct blow to the precordial area. Collapse is usually immediate, although there are isolated cases of collapse occurring after a brief period of consciousness. It is postulated in those cases that the initial rhythm may be ventricular tachycardia that degenerates into ventricular fibrillation. [5] [6] Cases have also been reported where the blow is to the left lateral chest wall, rather than to the precordium.[16]

Pathophysiology
The pathophysiology of commotio cordis is incompletely understood. It is known that there are 3 primary determinants that appear to play a key role in the induction of commotio cordis events. These are the location, the force, and the timing of the blunt chest impact.[4] [6] [11] [17]

As mentioned previously, the impact is almost always in the precordial area. In young victims, it is postulated that the narrow AP diameter of the chest, combined with increased compliance of the chest wall, come together to transmit an external chest wall blow to the underlying heart. As the body ages, the chest AP diameter increases, and compliance is lost, conveying a protective effect from such injuries.

The force of the blow is also thought to be a significant variable in the cause of commotio cordis. It appears that the risk of cardiac arrest after a chest blow is inversely related to the force of the impact,[6] [11] with force being a function of both the mass and acceleration of the object. In an experimental swine model, Link et al showed that the more forceful the missile impact to the chest, the more likely it was to induce ventricular fibrillation.[11] The experimental protocol developed by Link used objects of differing hardness, and clearly showed the relationship between missile density and propensity to induce arrhythmia.

Lastly, timing of the blow appears to be a critical factor in the induction of ventricular fibrillation. Again, Link's model showed that the blow to the chest must be delivered during the vulnerable period of cardiac repolarization. This occurs during the terminal 15 to 30 msec before the peak of the T-wave. Blows delivered at other times in the cardiac cycle did not result in malignant arrythmias.[11] Figure 1 shows induction of ventricular fibrillation when a blow is delivered during this vulnerable period of repolarization.


Fig. 1. Six-lead ECG showing the electrophysiologic and hemodynamic effects of an impact to the chest by a wooden object at 30 miles per hour, timed to occur 16 msec before the peak of the T wave (vulnerable period). Reprinted with permission from Link et al.[11] Copyright © 1998 Massachusetts Medical Society.



Of note, there have been case reports in which marked ST-segment elevation and bundle branch block morphology have been observed after blunt chest injury in survivors of commotio cordis sudden death events.[18] [19] This electrocardiographic morphology was also described by Link et al[11] in their swine model, and seemed to occur most frequently when the blow was delivered at other times in the cardiac cycle, specifically when it was timed to the QRS complex or other portions besides the terminal 15 to 30 msec of the ST segment (Fig 2).


Fig. 2. Six-lead ECG showing the electrophysiologic and hemodynamic effects of an impact to the chest by a wooden object at 30 miles per hour, timed to occur during the QRS complex (nonvulnerable period). Reprinted with permission from Link et al.[11] Copyright © 1998 Massachusetts Medical Society.


In case reports, this ST elevation has been ascribed to residual cardiac ischemia or coronary artery vasospasm. Link, however, found no evidence of either of these entities in animals showing ST elevation morphology. Link has further supported this in humans when he reported a case that showed normal coronary angiography in a resuscitated victim of commotio cordis who presented with marked ST elevation on electrocardiogram (ECG).[17] This is further supported by Bir et al, who showed similar findings in an early experimental porcine model of commotio cordis.[20] It is concluded by Link and Maron that the significance of ST elevation in this circumstance is unclear at present, but that cardiac ischemia is an unlikely cause.[6] [11]

Interestingly, this clinical picture of ST elevation in the absence of structural heart disease or coronary artery pathology has also been described in nontraumatic forms of sudden death. Brugada et al[21] [23] have documented episodes of sudden death or near sudden death in previously healthy patients who present with right bundle branch block, marked ST elevation in leads V1 to V3, but no structural disease and normal coronary arteries. Brugada's preliminary research indicates dysfunction at the cellular level involving the cardiac sodium channel, leading to this clinical constellation.[23]

Link et al have also implicated dysfunction of cardiac sodium channel as a possible causative factor in commotio cordis, linking the precordial blow with selective activation of the sodium-potassium (ATP) channel.[24] It is postulated that the blow during the terminal 15 to 30 msec of the T-wave transiently and selectively opens the sodium channel to potassium influx, resulting in marked increases in intracellular potassium, and subsequent ventricular fibrillation. Although this is also a preliminary finding, it is the first research to document a specific mechanism that could cause the syndrome of commotio cordis, and seems to corroborate Brugada's observations in nontraumatic situations.

Survival
The rate of successful resuscitation of victims of commotio cordis is low. Only 10% of the 70 patients reported in the commotio cordis registry survived their events.[6] Fifty-two of these victims were known to have had CPR within 3 minutes. Despite prompt resuscitation in patients with presumably disease-free hearts, only 11 subjects had a perfusing, organized cardiac rhythm restored. Four of these resuscitated patients subsequently died, leaving 7 (of 70) survivors (10%). Two of these 7 survivors had normal neurologic recovery, whereas 5 of the 7 were left with residual neurologic deficits. In summary, after an episode of commotio cordis, only 2 of 70 patients (2.8%) went on to a full recovery. [6]

Summary
Commotio cordis is a devastating electrophysiological event that occurs almost exclusively in young, healthy, and active patients who experience a blunt injury to the anterior chest. Experimental evidence indicates that such a blow, when delivered over the heart during the vulnerable period of cardiac repolarization, induces ventricular fibrillation and sudden cardiac death. Despite prompt resuscitative efforts, survival from such an incident is rare, and neurologically intact survival is even more rare.

References

1. Schlomka G, Schmitz M: Experimentelle Untersuchungen Uber Den Einfluss Stumpfer Brustkorbtraumen Auf Das Electrokardiogramm. S Ges Exp Med 1932;85:171-190

2. Meola F: Commozione toracica. Giornale Internazionale delle Scienze Mediche 1879;1:923-937

3. Maron BJ, Poliac LC, Kaplan JA, et al: Blunt impact to the chest leading to sudden death from cardiac arrest during sports activities. N Engl J Med 1995;333:337-342 Abstract

4. Maron BJ, Strasburger JF, Kugler JD, et al: Survival following blunt chest impact induced cardiac arrest during sports activities in young athletes. Am J Cardiol 1997;79:840-841 Abstract

5. Vincent GM, McPeak H: Commotio cordis. Phys and Sports Med 2000;28:31-39

6. Maron BJ, Link MS, Wang PJ et al: Clinical profile of commotio cordis: an under appreciated cause of sudden death in the young during sports and other activities. J Cardiovasc Electrophysiol 1999;10:114-120 Abstract

7. Denton JS, Kalelkar MB: Homicidal commotio cordis in two children. J Forensic Sci 2000;45:734-735 Abstract

8. Liberthson RR: Sudden death from cardiac causes in children and young adults. N Engl J Med 1996;334:1039-1044 Citation

9. Michalodimitrakis EN: Vehicular accidents and cardiac concussion. A traumatic connection. Am J Forensic Med Pathol 1997;18:282-284 Abstract

10. Burke AP, Farb A, Virmani R, et al: Sports-related and non-sports-related sudden cardiac death in young adults. Am Heart J 1991:121:568-575 Abstract

11. Link MS, Wang PJ, Pandian NG et al: An experimental model of sudden death due to low-energy chest-wall impact (commotio cordis). N Engl J Med 1998;338:1805-1811 Abstract

12. Estes NAM: Sudden death in young athletes. N Engl J Med 1995;333:380-381 Citation

13. Kaplan JA, Karofsky PS, Volturo GA: Commotio cordis in two amateur ice hockey players despite the use of commercial chest protectors: Case reports. J Trauma 1993;34:151-153 Abstract

14. Towbin JA: New revelations about the long-QT syndrome. N Engl J Med 1995;333:384-385 Citation

15. Viano DC, Artimann CG: Myocardial conduction system dysfunction from thoracic impact. J Trauma 1978;18:452-459 Abstract

16. Kaplan JA, Karofsky PS, Volturo GA: Commotio cordis in two amateur ice hockey players despite the use of commerical chest protectors: Case reports. J Trauma 1993;34:151-153 Abstract

17. Link MS, Ginsburg SH, Wang PJ, et al: Commotio cordis: Cardiovascular manifestations of a rare survivor. Chest 1998;114:326-328 Full Text

18. Link 1998, Wang JN, Tsai YC, Chen SL, et al: Dangerous impact-Commotio cordis. Cardiology 2000;93:124-126 Abstract

19. Crown LA, Hawkins W: Commotio cordis: Clinical implications of blunt cardiac trauma. Am Fam Phys 1997;55:2467-2470

20. Bir CA, Viano DC: Biomechanical predictor of commotio cordis in high-speed chest impact. J Trauma 1999;47:468-473 Abstract

21. Brugada J, Brugada R, Brugada P: Right bundle-branch block and ST-segment elevation in leads V1 through V3: A marker for sudden death in patients without demonstrable structural heart disease. Circulation 1998;97:457-460 Abstract

22. Brugada J, Brugada R: Further characterization of the syndrome of right bundle branch block, st segment elevation, and sudden cardiac death. J Cardiovasc Electrophys 1997;8:325-331

23. Brugada J, Brugada R, Brugada P: Sudden death in patients and relatives with the syndrome of right bundle-branch block, st segment elevation in the precordial leads v1 to v3 and sudden death. Eur Heart J 2000;21(4):264-265.

24. Link MS, Wang PJ, VanderBrink BA, et al: Selective activation of the K(+)(ATP) channel is a mechanism by which sudden death is produced by low-energy chest-wall impact (commotio cordis). Circulation 1999;27:100:413-418

[Sneaky SF Dude]

Originally posted by Doc T
tamponade in and of itself does not allow for enough blood loss to cause hypovolemic shock...the pericardium just won't stretch enough to hold that much blood. Now, if there is a hole in the pericardium that leaks intermittently into the chest cavity then that is another story all together.

the reason you see hypotension with a tamponade is because the pressure builds up in the pericardial sac and doesn't allow the heart to contract and distend normally leading to a very low cardiac output.

Volume challenges are actually recommended because augmenting the fluid going into the heart (preload) can actually cause it to fill better despite the increased external pressures {as already mentioned earlier as increasing preload}...so aggressive fluid management would be indicated both before and after pericardiocentesis in an effort to maintain a blood pressure/cardiac output.

doc t.

Do you agree with this? To me, the phrase "in an effort to maintain blood pressure" is key. I can't imagine it would take me long to perform the pericardiocentisis. I'm thinking let the blood pressure dictate my fluid therapy.

If it is commotio cordis, there's not much I can do about it in my environment.

[Doc T]

Originally posted by Sneaky SF Dude
Do you agree with this? To me, the phrase "in an effort to maintain blood pressure" is key. I can't imagine it would take me long to perform the pericardiocentisis. I'm thinking let the blood pressure dictate my fluid therapy.

If it is commotio cordis, there's not much I can do about it in my environment.

in commotio cordis you wont' have JVD... the situation you described (ie. Beck's triad) was what i was discussing and the discussion relly related to tamponade. I agree the BP is the key and dictates volume management...if someone is normotensive you don't need to volume load them but that is not the case if you have beck's triad, eh?

[Sneaky SF Dude]

Originally posted by Doc T
in commotio cordis you wont' have JVD... the situation you described (ie. Beck's triad) was what i was discussing and the discussion relly related to tamponade. I agree the BP is the key and dictates volume management...if someone is normotensive you don't need to volume load them but that is not the case if you have beck's triad, eh?

Agreed, but if I have Beck's Triad, I'm going to do the periocardial centisis and then I almost immediately won't have Beck's Triad anymore, right? My understanding is that the results are almost immediate?

[Doc T]

Originally posted by Sneaky SF Dude
Agreed, but if I have Beck's Triad, I'm going to do the periocardial centisis and then I almost immediately won't have Beck's Triad anymore, right? My understanding is that the results are almost immediate?

in a perfect world you do pericardiocenteses immediately but in real life it takes you time to get all the stuff together, at least it does in the trauma bay where we don't keep the stuff out on a tray since we rarely use it.

in the field i'd imagine it take longer but maybe i am wrong.

in the meantime, as soon as the suspicion arises and beck's triad is noted volume should start in an effort to keep your patient from arresting.

and yes, results are immediate...its is truely amazing...

are you able to leave pericardial catheters with the equipment you have in the field or is it simply a long needle?

[Sneaky SF Dude]

Originally posted by Doc T
in a perfect world you do pericardiocenteses immediately but in real life it takes you time to get all the stuff together, at least it does in the trauma bay where we don't keep the stuff out on a tray since we rarely use it.

in the field i'd imagine it take longer but maybe i am wrong.

in the meantime, as soon as the suspicion arises and beck's triad is noted volume should start in an effort to keep your patient from arresting.

and yes, results are immediate...its is truely amazing...

are you able to leave pericardial catheters with the equipment you have in the field or is it simply a long needle?

"in real life it takes you time to get all the stuff together" LOL - Doc, if an 18D doesn't have his stuff together all the time, he's Team Leader/Team Sergeant sends him ruck bowling long before he treats a patient. It would probably take me less time to do a pericardial centisis than to start an IV.
I was taught to do it with an IV catheter. Of course if I had a teammate with me (which I always try to do) I would have him start the IV and I would do the centisis. I would probably run the IV run the IV full open until I could check vitals. I'm not arguing with you. Its just that I was taught from the school of run two large bore IVs wide open for everything. Research is making me rethink that philosophy. Is there the possibility that aggressive fluid therapy could re-cause the tamponade?

[Doc T]

Originally posted by Sneaky SF Dude
[BIts just that I was taught from the school of run two large bore IVs wide open for everything. Research is making me rethink that philosophy. Is there the possibility that aggressive fluid therapy could re-cause the tamponade? [/B]

it has been hypothesized and shown in animal models that if you raise the BP with volume resuscitation the animals will bleed more. That said, Mattox in dallas tried to do the study on trauma patients and got IRC approval (although no one is quite sure how) to do this study... half got IV resus and half didn't. When they looked at the data what they found was that in the subset of patients with penetrating chest trauma the group that got no resusc in the field did better... but when you look at the data the arrival BPs were not significantly different and the patient numbers were not very large allowing for statistical errors...also they had VERY short transport times.

In short, in my opinion it is a bad study that often gets quoted because its what people wanted to believe. The other groups (the majority of patients) had no difference in outcomes... and it was only subset analysis that identified the chest group.

and yes, the patient will probably retamponade...whether you resuscitate or not.... he tamponaded the first time with no help...its the nature of the injury....hence the need for the catheter so you can intermittently draw off fluid as needed.

btw...where do you keep all the stuff you need? in a pack? that's filled with everything...? I am asking for real since I don't know...how do you organize it all? like a diaper bag with different compartments for different things? Can you really find everything you need but rarely use that quickly?

doc t.

[Sneaky SF Dude]

I saw that study and agree, it doesn't tell us anything.

Different guys carry their stuff different ways. The approved Army method is a large bag (M5) inside a larger pack with other gear. Most medics carry some key equipment in other places - on a vest, in a pocket. Some wear specially designed medic vests. Believe it or not, how to carry this stuff is always an ongoing discussion. I always had IV kits and needles in various pockets and pouches. Team members also carry them.

Top left shirt pocket you will always find a plastic spoon and on medics, you could hold them upside down and shake them and an ER's worth of stuff would fall out. Engineers, it would be blasting caps and det cord, commo men-batteries and wires. Weapons men still haven't figured out that there are pockets on the uniforms. :D

[Doc T]

[i]
Top left shirt pocket you will always find a plastic spoon :D [/B]

why?

[Sneaky SF Dude]

You never know what a brother will have cooking in a canteen cup if in the rear area or who will offer up som LRRP ration if in the field. Never miss a chance for chow.:D

[CPTAUSRET]

Originally posted by Sneaky SF Dude
You never know what a brother will have cooking in a canteen cup if in the rear area or who will offer up som LRRP ration if in the field. Never miss a chance for chow.:D

Sweet:;)

[Doc T]

Originally posted by Sneaky SF Dude
You never know what a brother will have cooking in a canteen cup if in the rear area or who will offer up som LRRP ration if in the field. Never miss a chance for chow.:D

lol... okay... was trying to figure out what you could do emergently with a spoon...didn't figure the answer was eat...

doc t.

[Sneaky SF Dude]

I KNEW I'd get you with that one :D

I can just see you sitting there thinking "What the hell is that crazy bastard doing with a plastic spoon during a pericardial centisis?"

[CPTAUSRET]

Originally posted by Sneaky SF Dude
I KNEW I'd get you with that one :D

Sneaky:

You were trolling::D

Terry

[Sneaky SF Dude]

Naw Cap, just keeping the Doc awake and making sure she has a good time. Don't want her to wander off on us.

[CPTAUSRET]

Originally posted by Sneaky SF Dude
Naw Cap, just keeping the Doc awake and making sure she has a good time. Don't want her to wander off on us.

Sneaky:

We normally are in agreement, but on those thoughts we are in total "lockstep":;)

Terry

[Doc T]

Originally posted by Sneaky SF Dude
Naw Cap, just keeping the Doc awake and making sure she has a good time. Don't want her to wander off on us.

i am awake! but am on service this week.... but trying to keep up.... 16 ICU patients and another 20 on the floor.... pays the rent though.....

doc t.

[Sneaky SF Dude]

Nothing like a full load huh Doc? I feel for you.

[Axe]

Not that you had not already, Doc T, gained my respect, but you just did by mentioning your patient load.

I feel burdened when I have five of my family members that I am caring for for relatively minor aliments. And I know they won't be taking me to court!!!!

You are the WOMAN!!

I talk daily to my internist friend and listen to his bitches. He does work hard, but his biitches make me think about how you have to handle the load and then some every day. I tip my hat to you. Thank goodness we have docs like you who will handle their weight and then some!!

I don't clearly know where you are located, but if I ever become a trauma pt, I hope I go under your knife. I will sign a complete waiver in advance, before analgesia.

This is the ultimate compliment coming from me.

Good pulses, and good cutting,

Rick Louys

[Doc T]

Originally posted by Sneaky SF Dude
Nothing like a full load huh Doc? I feel for you.

it makes the day go by quickly.... overwhelms the residents at times but they do a pretty good job. Not sure i'd love my job as much as I do without them.

it certainly teaches you to be organized.

[RsovRanger]

I am going to show you at least how generally I pack my kit, so you can see a general idea... gonna post 2 pics as well...

Medical assault vest, left to right as worn, my rig:

Ammunition, 6 30 round magazines
oral/nasal airways, aschuman chest seals, 10g needles for decompression
iv starter kits w 2 18g's, saline lock, tegaderm, couple alcohol pads
Stahl rolling torniquets
casualty cards
saline for flushing locks
kerlex, emergency bandages, ratchet tornequits
blue green red and IR chemlites
inside the vest I usually have a couple minichems, cans of cope, alcohol markers, IR strobe, trauma shears, sharps shuttle, medic handbook


Assault pack, outside then inside, top to bottom

Top outside pouch:
oral/nasal airways, intubation kit, combi-tube. cric kit, ashuman chest seals, decompression sets

bottom outside pouch:
kerlex, emergency bandages, tornequits

inside pouches:
bvm, narcs, chemlites, hespan/NS iv sets, camelback, minor wound care kit, FAST-1, chest tube set, rehydration drink packets, sharps shuttle, medications, epi-pen, snakebite kit, needle sets for drugs, spare junk tucked away

back mesh pouch:
ace wrapss, coban wraps, sam splints, emergency blankets

outside I have trauma shears and a maglite, usually have a overt light mounted on my helmet but tuned so it's bright enough for me to work but not enough to get me shot at more than I need...


some shit i prolly missed.. gps, compass, more cope, etc, but that's the General rundown.

[RsovRanger]

Aid bag picture

[Sneaky SF Dude]

Show the aid bag open.

[CPTAUSRET]

Originally posted by Sneaky SF Dude
Show the aid bag open.

Yes, please:

Terry

[Sneaky SF Dude]

He can't, he took it off the internet. Its from the manufactuer's website.LOL

[RsovRanger]

Ok... I don't have mine in my room, but I'll make you a shitty ass drawing so you can get an idea of what it looks like.
The aid bag clamshells down the back, so you can open it up flat and have access to everything. This is a top view of all the pouches...

[Doc T]

Originally posted by RsovRanger
Ok... I don't have mine in my room, but I'll make you a shitty ass drawing so you can get an idea of what it looks like.
The aid bag clamshells down the back, so you can open it up flat and have access to everything. This is a top view of all the pouches...

thank you very much.....

[troy2k]

RSOV, my compliments on choosing Tactical Tailor. I love their shit. Just ordered the 2 piece version (opens in front) of the same rack you showed, as well as their X-harness for the back straps, so now the whole ensemble slips on like an LBE. Wears like a dream over body armor, no more straps slipping between my neck and the RBA.
Great load out as well. Have you guys got the Hemostatic dressings yet?

[RsovRanger]

yeah, use hemicon fibrin bandages for wounds deserving of a limited asset.