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crushing case

Brandon Oto brandon at degreesofclarity.com
Sun Apr 15 03:24:58 BST 2012


My understanding was that with sufficient muscular damage, the effects can be very rapid -- secondary to traumatic release of burst skeletal muscle contents into the circulation, not to peripheral hypoperfusion.

Exertional rhabdomyolysis periodically presents among the athletic population following very intense exercise of a damaging nature (i.e. high-volume eccentric contractions); workouts of under 20 minutes can easily produce this syndrome.

Brandon

***
http://degreesofclarity.com/
http://emsbasics.com/




On Apr 14, 2012, at 7:33 PM, Jeff Anderson wrote:

> Dr. Hardcastle,
> The scenario, as I read it, has the worker being removed from the ground
> fairly soon after he was crushed.  Is this enough time for crush syndrome
> and reperfusion to be an issue?  I thought it took hours of anaerobic
> metabolism to produce the acidosis and hyperkalemia that would lead to
> PEA.  Am I missing something?  Thanks
> 
> Jeff Anderson
> Bossier City, LA
> 
> On Wed, Apr 11, 2012 at 6:35 AM, Dr and Mrs T Hardcastle <
> dr.tchardcastle at absamail.co.za> wrote:
> 
>> Caesar - my comments between your questions:
>> Tim Hardcastle
>>> A case submitted for your consideration:
>>> 
>>> 43 yo male construction worker suddenly had large amount of gravel, rocks
>>> and dirt fall on him, burying him up to his neck.  Co-workers dug him out
>>> with shovels (took them ten minutes) and he remained awake and alert
>>> during
>>> this time.  Finally freed of the rubble he collapsed and lost
>>> consciousness.
>>> 
>>> Paramedics arrive  two minutes after his collapse.  No bystander CPR is
>>> being performed.  He has no palpable pulses or spontaneous respiratory
>>> efforts.  Pupils reported as 5 mm bilaterally and unresponsive. The
>> medics
>>> begin closed chest compressions, place him on a spine board and load him
>>> into the ambulance.  They perform rapid sequence intubation (successful
>> on
>>> first try) and start two IVs en route to the hospital.  They give two
>>> doses
>>> (1 mg) of IV epinephrine en route to the hospital.  They do not feel
>>> return
>>> of palpable pulses.  Transport time is 16 minutes.
>>> 
>>> On arrival to ER he is undergoing closed chest compressions.  He still
>> has
>>> no palpable pulses at the carotid or the femoral arteries bilaterally but
>>> on ECG monitor his *heart rate is 140/min*.  The endotracheal tube seems
>>> to
>>> be in the correct position on visual inspection with the laryngoscope
>>> (i.e.
>>> it is going through the vocal cords). He has bruising and abrasions of
>> the
>>> chest wall but no lacerations or external bleeding.  Rib fractures are
>>> palpable bilaterally. Breath sounds are equal bilaterally and he is easy
>>> to
>>> ventilate using the bag-valve.  There are two 16 gauge antecubital IV
>>> catheters already in place and one of the medics is squeezing in a bag of
>>> 0.9 NS (they have given 300 ml so far).  Total pre-hospital CPR is
>>> estimated at 20 minutes (includes time at scene and transport time to
>> ER).
>>> 
>>> What would you do at this point?
>>> 
>>> Would you:
>>> 
>>> A. pronounce him dead on arrival?
>> No
>>> B. continue closed chest compressions, give more fluid (crystalloid?
>>> blood
>>> products?) and intravenous epineprhine or other vasopressor?
>> Yes and check blood gas POTASSIUM and IONISED CALCIUM: this is an acute
>> reperfusion - typically occurs about 10 minutes to one our after release.
>> The underlying "tachy" PEA fits with hyperkalemia
>>> C. insert bilateral chest tubes?
>> Not empirically
>>> D. perform ER thoracotomy?
>> NO
>>> E. a combination of one or more of the above?
>>> F. something else entirely?
>>> 
>>> Thank you.
>>> 
>>> C. Ursic, MD
>>> Honolulu
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