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 ARCHIVES
TRAUMA-LIST |
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Traumatic Arrest : Gunshot abdomen (hypothermia, coagulopathy, acidosis)
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From: Karim Brohi, Royal London Hospital Approximately 20 year old is brought in by ambulance in the early hours of the morning. Gunshot abdomen. Entry? wound just to the right of the umbilicus. Exit? wound in the right buttock. No blood pressure but palpable pulse with ambulance crew who have scooped & run. Pupils equal & reacting. GCS 3 In the emergency room has a palpable pulse for about a minute and then loses it. What now? Karim
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From: Tom Scaletta Perform ED thoracotomy, cross-clamp aorta, transfuse type O blood, and get to OR ASAP. So, what's the twist?
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From: Dr. Mark Forrest Dear Tom, Wow! Do you wear your underpants over your trousers, blue-leggings and a cape....love your aggressive, no fuss approach...will you come and work in our hospital?!!! I agree though, what little twist does karim have up his sleeve?? Mark F, UK
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From: Walter Mauritz If I read this correctly your patient is in exsanguination cardiac arrest (what did the ECG monitoring say?) If this is the case you have two options: a) do nothing. Chances of success are 0%. Chances of success are approx. 1%. Best wishes Walter |
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From: Karim Brohi Yes well I went for option 2. Opened the chest via left lateral thoracotomy. No blood, no tamponade. Heart very empty. Still beating but at around 40/min. Now I'm not usually a fan of cross-clamping the aorta - there seems to be little evidence to support it. Anyone disagree? Nevertheless a couple of minutes trying to fill him through a 7.5F trauma line did very little so X-clamped the aorta at the diaphragm. Subsequently filled him (packed cells only) and managed to get the heart going again with palpable carotid pulse. Abdomen is very distended. Diaphragms are bulging into the chest and blood pouring out the gunshot wound. We go to the operating room. At laparotomy he has about a 3L haemoperitoneum and large central and pelvic retroperitoneal haematoma. He gets 4-quadrant packing a left medial rotation (Cattell) and X-clamp aorta below the renals, right medial rotation (Cattell-Brasch) reveals gunshot to the right internal iliac artery & vein at the bifurcation. Bleeding is audible. IVC clamped. Control distally of external iliac. Internal iliac divided to get to internal iliac vein which is ligated. Internal iliac subsequently ligated and orifice at iliac bifurcation oversewn. (Difficult) Also has 6 holes in the small bowel & 2 in the mesentery. Stapled resection. Packs to pelvis and raw areas. Laparostomy fashioned and thoracotomy closed. Total laparotomy time around 1 hour 15 minutes. NOW. He has had around 20 units packed cells, 10 of FFP, 2 pools platelets and some cryoprecipitate - all warmed via the Level 1 rapid infuser. (And 7.5mg Factor VIIa - sssshh!). His temperature is 33.7. Base excess -25. pH 6.73. He's is possibly beginning to clot. Goes to ICU. Here he continues to ooze and gets blood & FFP replacement. However over the course of the next 2 hours his temperature drops to 31 C. His clotting suddenly goes now out of control and he is unsalvageable. Dies after a lot of hard work and money. Anything you would have done differently? Would you have core re-warmed with bypass or A-V re-warming? What is the value of clotting assays in the presence of hypothermia & acidosis? Was he a lost cause from the outset? Should we have gone for Walter's option 1? Karim
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From: Eric Frykberg MD You did what you could--and have added a bit more evidence that there are times in which clamping of the aorta in this setting may work. The results are dismal only because the patients requiring it are dismal hopes with lethal injuries--that is not an indictment of the procedure, only of the injury. ERF
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From: Mark Forrest Dear Karim, Great effort and impressive operating time considering his injuries and likely chance of survival from admission. A few more questions rather than answers! How long was he without significant cardiac output and what
was the total cross clamp time? We discussed similar re-perfusion problems secondary to prolonged crush syndrome some time ago. Anyone got any new ideas? Regards
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From: Dan Caruso To Dr. Forrest and Karim, First to Karim... great effort to say the least... and I'll agree with Dr. Fry, probably not going to survive but great effort once again. Second to Dr. Forrest... we are working with CRRT (specifically CVVHDF)... difiltration along with venous warming on both ends of the circuit... And have utilized CRRT "early" in burn/trauma/crush patients with very good results. Dan Caruso
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From: Walter Mauritz Karim, Your ER and OR management of this case was exceptional! According to the largest published series of similar cases the chances to get this patient out of the ER alive were about 26%, and his chances of survival were 10% (because he made it to the OR). The overall chance of survival for these patients was 2.6% in the reference study (see below). If I read this correctly in the ICU the major problem was to keep BT above 32 °C. Our strategy would be: - External rewarming (w. Bair Hugger or similar device) - Fluids and PRC warmed to 39 °C before in/transfusion - ventilation gases heated to maximum I assume that your ICU team did this; if these techniques failed to maintain BT there are no options left. Forget clotting parameters if the patient goes into hypothermia < 32 °C. NB: There is no evidence (i.e. multi-center randomized blinded trials - but these would be somehow difficult, I think) that cross-clamping the aorta in these cases is beneficial, but do we really need evidence for treatment strategies that are simply logical? You did well, Karim, and your patient was just unlucky, probably. Best regards, Field triage of the pulseless trauma patient.
HYPOTHESIS: Trauma patients who are pulseless
at the scene of injury and whose electrical cardiac activity
is less than 40 beats/min cannot be revived. DESIGN: Retrospective
review. |
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From: Mark Forrest Dear Dan, Interested to hear more about your CVVHDF work, in terms of your set-up, exchange regime and time started. Have you ever started it before removal of cross clamp or MAST suit (if evacuated from crush-site with one applied)? Regards, Mark F
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From: Caesar Ursic >Would you have core re-warmed with bypass or A-V re-warming? Probably. At a core temp of 31 C, he's never gonna clot well, and the group in Seattle (Jurkovich, et al) did show some success with their A-V circuit running through the Level One infuser (although their overall mortality was NOT statistically different, their early mortality was less in the active core rewarming group). >What is the value of clotting assays in the presence of hypothermia & acidosis? Minimal. Cold blood won't clot in a cold patient - at least one this cold, even though it does clot nicely once the lab assay machines warm it up to standard conditions (37 C, I believe). >Was he a lost cause from the outset? Should we have gone for Walter's option 1? I'm sure you've saved a few patients with similar injuries and presentations, as most of us have. Each case is unique, in a sense, in that predicitng outcome is difficult when using data from comparitive groups. He had signs of life when you got him, so the attempt was justified, IMHO. No signs of life (fixed pupils, no pulse, no sinus rhythm above 40) = D.O.A. where I work. C. Ursic. M.D. / UCSF-East Bay / Oakland, CA, USA
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From: Karim Brohi If I read this correctly in the ICU the major problem was
to keep BT above Walter - I think we lost control of this case because we lost
control of his I do not believe that the Bair Hugger does anything positive
if you are Forget clotting parameters if the patient goes into hypothermia < 32 °C. - I agree - so we 'best guess' and pour in the clotting factors
given the You did well, Karim, and your patient was just unlucky, probably. Thanks - but we had control of this guy and we lost it. I've
seen it We are not aggressively core re-warming at present. I cannot
think of Karim |
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From: Karim Brohi Mark, He probably had a few episodes of between 2 and 5 minutes without Total cross-clamp time was around 65 minutes, 30 minutes above
the Why did he cool? I don't think fluids were warmed as aggressively
on ICU as Serum K+ and Ca2+ I don't know off hand. When cross-clamps were removed there was very little change
in his Karim |
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From: Walter Mauritz I do not believe that the Bair Hugger does anything positive
if you are
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From: Eric Frykberg We are not aggressively core re-warming at present. I cannot
think of
Why did he cool? I don't think fluids were warmed as aggressively
on ICU as No--read some of Larry Gentilello's work--the cooling is a
natural protective response of the body to severe injury, shock,
sepsis, etc--it is a bit arrogant to think it is all our fault,
implying it is us who are in total control and have total understanding
of the body, something we constantly find out we are wrong about
(remember bloodletting? Our first President was killed by it--but
the doctors blamed themselves for not having let out more!)
Think about it Karim..... |
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From: John A Arts Dear members,There's one thing we should NEVER forget: Despite our experiences and education,we'll NEVER be able to save everyone! Being a cardiac surgeon,I saved lots of lives,but also LOST some lives,some of them " mors in tabula". Despite our titles,stethoscopes,OR's,ER's,high-tech equipment,let's be thankful for the ones we CAN save!! THAT'S what we stand for!!!.. Happy holidays, |
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From: Mark Forrest Dear Karim, Further on the warming issue, I have to agree that the Bear
hugger is rarely Other thoughts for discussion / future: -what were your target blood pressures once the clamp was on? -I am sure that hypertonic saline/dextran would have allowed
you to restore Still a great case Karim and I fully understand your frustrations
when you Regards |
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From: Dan Caruso Doctor Forrest and Friends... Too busy for words these days... Sorry for the delay in responding...
But, have used in crush syndrome, both in late stages and "early" with patients that still have 30 - 50 cc/hr urine output and slowly rising CPK.... going to get some questions on that one for sure... and also have used "early" with crush/rhabdo and CPK 100,000 and greater. Can lower CPK and Creatinine better than any ole mannitol/bicarbonate drip. It just simply works great in those situations. Now, more to your questions... It would take quite awhile to discuss our set up but I can tell you quickly that we run everything (replacements etc...) pre filter, always use sodium citrate (NO HEPARIN) and have found the T- 60 to be a much better filter than T-100... Blood speed always hoped to be 135 (best creatinine clearance) and dianeal at 800 cc/hr. We have hot lines on return to patient and into the pump and have found we can raise temp quickly in this manner... Also, filter life, across the board in burn/trauma/vascular/ped/neonatal and cardiac patients is about 24 hours. For example, have used CRT in early burn resuc or trauma resuc and can maintain and/or move core temp 2 - 3 degrees within hours... Am working on some science to these statements... Of course, will use with bear hugger, hot lines on other IV's, over head heaters etc... More fascinating is the degree in which we can maintain PAWP/CVP 16 to 20, use CRT to pull off extra-vascular fluid, decrease FiO2 requirements, correct acidosis, and of course difiltrate (lower creatinine) while decreasing overall fluid intake in large burn/trauma resuc! Amazing piece of equipment... have a great CRT nurse, Roger Gilbert, who has Master's Degree thesis on CRT! If you want to know more be glad to talk at ya! Thanks Dan Caruso |
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From: Karim Brohi I don't think we are blaming ourselves. What we're trying to
do is get better. |
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From: Karim Brohi Mark: Other thoughts for discussion / future: Hmm - possibly but our ITU is only 30 yards from theatres and
it's probably -what were your target blood pressures once the clamp was on? A palpable carotid in resus. After that I hope we were going
for around 70 -I am sure that hypertonic saline/dextran would have allowed
you to restore Possibly - but mightn't this contribute to his acidosis later? -prior to clamp removal he needed some mannitol, bicarb
and probably He had some bicarb (more for his acidosis - pH 6.7) but no
calcium or
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From: Eric Frykberg I for one applaud your efforts, and your soul-searching for an answer, and am not discouraging this at all--that's how progress happens. It is a simple opinion on my part though that you will not find the answer you seek here--if you do, let the rest of us know? However-- One thing to add to your idea of finding a better way than sending labs off and waiting, though is to think about a massive transfusion protocol, as we instituted about ten years ago . We published the protocol if you wish to see it, and think it greatly streamlines obtaining blood products and labls in settings such as you had. We reached an agreement with the bloodbank to do away with much of the administrative paperwork and procedures when massive trasfusion is necesary (i.e. more than 10 units within a few hours)--only one blood clot in the beginning then never again, starting with 4 units O neg, then automatically sending up MTP "packs" every 20 minutes in an ice coooler (each one with 5 units PRBC's, 2 units FFP and 10units platelets of type specific only), requiring only one rather than two signatures to verify before transfusion, obtaining a fibrinogen level after each 3 MTP packs and adding cryoprecipitate to the next pack only if fibrinogen< 100, and sending INR and platelet count after each 4 packs--all automatic and done by the blood bank, allowing the surgeons and anesthesia and OR personnel to concentrate on their jobs, all to keep going until the protocol is specifically terminated, by the same physician who started it. Only a very small number of docs are authorized to ever start one. No efforts to crossmatch are to be made until after the protocol stops--that is a real waste of expense and effort in a true massive transfusion. If more than 10 units of O neg are initially transfused, then that is all that is given thereafter. This is all based on solid data from the literature for validity and efficacy--and works! It is much like the change in mindset we must have for a mass casulaty event from our normal everyday treatment of individual patients--the normal procedures for transfusion just will not work in this setting , as we all know--way too burdensome. So some small sacrifice of risk of transfusion reaction is made to prevent a much more urgent problem--loss of life! There is no need at all for cross match so don't do it! We have yet to see a single transfusion reaction after ten years--and it is not a great strain on resources as one of these is called maybe 3 or 4 times/year on average--and we all sit down and analyze what happened after each one, to help work out the bugs and fine tune the procedures. There is a pretty solid literature on this concept, which I will supply if you wish--and if you want to try it, get everybody in the OR and blood bank on board, and also inservice anesthesia--in our place we all swear by it once we all realized the advantages, but it takes a lot of maintenance to keep current. Some changes in our protocol have been made, but the basic concept remains the same. In fact, OB-gyn and medicine have used it occasionally for massive bleeds as well, so these services will also need inservicing. One caveat--don't interfere with the blood bank during such a protocol, so if any rogue doc cannot restrain themselves from thinking they know better, and calls the bloodbank for more FFP, blood, or any other product outside of protocol etc, the protocol automatically terminates and the usual slow, chaotic and bureaucratic mess is then reverted to. Happy holidays! ERF Trauma Quarterly 10:12-31, 1993. Frykberg ER et al. Massive Transfusion: history, pathophysiology and management. |
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From: Walter Mauritz Karim, |
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From: Dan Caruso Karim, Best way I can explain, somewhat of the unexplainable is a current case scenerio... We normally use it in the ICU phase although in this patient it is in the ICU/OR phase... 62 y.o. diabetic with nec fasc involving in 30% TBSA... debrided
x 2, CPK's > 100,000, anuric, creatinine of 3.5, on Levophed
and Dobutamine... Anyway... PAWP 28, CVP 24, CO 5.2, CI 3.4, SVR 400, SI 30.0,
SvO2 68 with Interestingly, clinically not in pulmonary edema like many of these patients end up but quite edematous and echo shows EF 35 - 40% with "full" ventricles, no valve disease Now, on CRRT (specifically CVVHDF) and all I can tell you is that once we start we initially keep patient I = O and then slowly start to remove fluid (50 - 100 cc/hr) since we know patient "fully-tanked" by CVP/Wedge and ECHO results... In our experience, over several days, with the CRRT, we can closely keep track of wedge and CVP since we can remove or add fluid at a whim... And for reasons, I cannot explain, we are often able to at least sustain these patients and wean off the vasopressors (most likely due to treating the other underlying issues of sepsis, necrotic tissue, use of antibiotics etc...). Finally, we will get this patient to a Wedge/CVP of 18 - 20 and then keep I = 0 but with insensible loses, she will continuely to slowly diuresis fluid (I presume from extravascular areas)... Anyway... we then keep going with CRRT to treat rhabdomyolysis and acute renal failure until resolved! My nurse manager, Roger, and myself have been on the "circuit" especially burn arena, speaking on this subject... Lots of interesting looks and thoughts from others... I don't have all the answers by a long shot but I can tell you that I look at the CRRT as the "third kidney" in which one can filter blood (? cytokines) as well as precisely manage fluid status, electrolyte status, acid/base status, etc... In the correct hands, the technology I feel can be quite helpful! I hope this helps Dan Caruso |
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From: Ian Civil Dear Karim, We use the TEG [thromboelastograph] here in Auckland because
it is available with the liver Ian |
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From: Mark Forrest Dear Dan, |
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From: Mike Walsh Dear list Karim and I are trying to improve the outcome for these young
people. Over the I think that the suggested transfusion protocol, better warming
techniques, Mike Walsh |
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trauma.org 7:2, January 2002
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