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Wed Dec 20 14:25:11 GMT 2006

Jason

Good to see you contribute and appreciate your views. Is there any evidence regarding time of entrapment and extent of entrapment (eg complete limb under wall vs body caught in crashed car, with minimal pressure on limbs) in terms of severity and treatment protocols. You did not mention Carlos Brown's work from LAC. They showed that for CK <15000 the incidence of renal failure was <6% and that bicarb and mannitol had no advantage over saline flush alone. This is my experience here in South Africa too; one of my registrars is writing up our series of close to 500 cases of crush over a two year period at the moment for his M.Med dissertation.

I agree on the exchange resins though, although this effect seems related to longer term rather than acute lowering of the potassium.

The majority of crush injury I see comes from interpersonal violence (locally called kangaroo-court and sjambok assault, you may remember) and from vascular injury reperfusion. Is the effect and outcome different?

The incidence of chronic renal dysfunction in this group is surprisingly small from what my renal unit colleagues, who follow these patients longterm, tell me. If they reverse the renal dysfunction (usually within around three weeks) they seem to have good functional outcomes with a small group having persistant hypertension at five years. the trick is to not let them get dehydrated during the inevitable polyuric phase of recovery.

Regards
Tim
Dr T C Hardcastle
M.B.,Ch.B.(Stell); M.Med(Chir); FCS(SA)
Senior Surgeon / Senior Lecturer: Surgery (Trauma and ICU)
ATLS  instructor and DSTC Cape Town Course Director
Intern program Coordinator: Surgery
M.Med (Emergency Medicine) Executive Committee member
Clinical Head (Director): Diana Princess of Wales Trauma Unit
Division of Surgery (General) Room 4064
Department of Surgical Sciences
Tygerberg Hospital / University of Stellenbosch
PO Box 19063
Tygerberg 7505
Western Cape
South Africa
e-mail: tch at sun.ac.za
Cell: +27824681615
Office: +27219389281 or 4911 pager 0302

-----Original Message-----
From: trauma-list-bounces at trauma.org
[mailto:trauma-list-bounces at trauma.org]On Behalf Of Jason Van der Velde
Sent: Tuesday, December 19, 2006 5:06 PM
To: trauma-list at trauma.org
Subject: Crush and tourniquets

You probably knew Karim that I would eventually resist no 
more and rise to your initial posting!!!  Time to stop 
lurking in this fascinating tourniquet debate!!

Apologies for the lengthily reply, but particularly in 
light of Dr. Mazur insightful comments, this is not a 
simple topic and needs space to be addressed properly. I 
believe I write with reasonable authority as apart from my 
clinical work, I lecture extensively on the systemic 
sequalea of muscle damage. It is the subject of my masters 
thesis, and in more detail my envisaged PhD work.

1st an observation: We are a large multidisciplinary 
discussion group. Equally trauma is NOT the remit of only 
one specialty or professional group. Predictably we all 
are approaching what is essentially THE SAME kinematics 
and pathophysiological process from different angles, 
which is not necessary a bad thing, but may I suggest that 
we all need to "think out of the box" that is our 
"individual specialties". This is particularly important 
for the patient, who's journey is a lifetime, and not the 
15min in the ambulance or 2 hours on the operating table. 
Crush syndrome kills or seriously disables:
1)      on or shortly after extrication (Cardiac 
Arrhythmias/thromboembolic)
2)      In a few days or weeks (Acute Renal 
Failure/Cardiac Arrhythmias/thromboembolic)
3)      In a number of years, which as acute clinicians we 
frequently forget! (Chronic Renal Failure)

Crush syndrome is a true systemic insult. Apart from the 
well know renal complications of muscle damage, 
prehospital deaths post extrication secondary to cardiac 
arrhythmia, are frequently misdiagnosed as hypovolaemic 
arrests and could hold a key to making a significant dent 
in post extrication mortality statistics, ie. Peak 1 of 
either the Scottish Trauma Audit[i] or Trunkey's[ii] 
curve. Hence this is an important subject that requires a 
roadside to critical care approach to management.

Electrolyte abnormalities occur frequently in patients 
with crush-related acute renal failure.[iii] We have known 
about such disturbances for some time now, particularly 
the tremendous potential for hyperkalaemia and consequent 
fatal cardiac arrhythmias.[iv] What we have not fully 
appreciated until quite recently is the staggering 
percentage of patients who have died either on scene or 
en-route to hospital, as a result of electrolyte 
abnormalities during or shortly post extrication.

Important autopsy findings from 111 deaths in the 1999 
Athens earthquake have only recently been made public.[v] 
Although this study's main purpose was to audit emergency 
response as a whole, it begins to give us the first real 
evidence to support a long held belief of the adverse 
effects of extrication on cardiac function. Researches 
from the University of Athens General Hospital evaluated 
and combined demographic data, circumstances of death, 
rescue time, mechanisms of injury, causes of death, 
Abbreviated Injury Scale (AIS 90) and Injury Severity 
Score (ISS) values, vital functions and co-morbidity in a 
study seeking to identify preventable deaths in Trunkey's 
first group. Their findings attributed a staggering 46.6 % 
of post extrication earthquake deaths directly to cardiac 
complications.

It is hypothesised that this pathophysiological process is 
far more common than we think in every day trauma practice 
and if this is so, it is clear that we have to drastically 
alter our current practices, particularly our prehospital 
practices, if we are to make any headway in addressing 
mortality/morbidity.

Dr. Mazur has certainly presented this list with a very 
logical approach to management. Perhaps I can add to his 
comments by providing some additional points as well as 
some evidence to back his management strategies up. The 
goals are prevention and protection. There is more than 
sufficient data to warrant an initial aggressive approach 
to preventing fatal cardiac arrhythmias, whilst at the 
same time initiating early, renal protective strategies. I 
am more than happy to discuss this data further, in depth, 
off list.

EARLY identification of at risk patients and assigning 
them to a crush protocol is the key. Crush protocols are 
not new. We've been studying them and using them since the 
1st world war![vi] Now I can safely make the comment that 
by the time you have biochemical diagnosis (ie. Serum CK) 
of a crush syndrome, it is too late. The decision to 
initiate preventative and protective strategies should be 
a balanced, educated decision weighing up kinematics, 
degree and time of entrapment, environmental influences 
and premorbid health against the need for circulating 
volume preservation and haemorrhage control.  The early 
use of myoglobin specific urinary dipstick appears to be a 
sensible tool in aiding such an early management 
decision.[vii].

I believe that the key is proper training and experience 
in identifying at risk patients by the kinematics of 
insult alone... How this is done is a whole discussion on 
its own. It is also a contentious issue at the heart of 
how we manage our prehospital emergency services. But what 
is NOT contentious is the overwhelming evidence:

Early aggressive intervention,[viii],[ix],[x] prior to 
extrication[xi], has been shown to benefit long term 
outcome in entrapped casualties at risk of Crush Syndrome.

WHY prior to extrication??
A NORMOvolaemic, NORMOtensive, NORMOthermic, NORMOetc. 
etc. etc. system handles the "ischemic soup" that is 
bolused from a released limb far better than one that is 
in haemodynamic crisis... If we are going to remove a 
crushing force or remove a tourniquet, the body has to be 
in shape to handle it! I speak from an anaesthetic 
perspective where I manage tourniquet release post 
operatively on a weekly basis both electively and as an 
emergency. Maintaining systemic normality is standard 
perioperative management in orthopaedic, vascular, 
plastics etc. etc. surgery. Can you all put hand on heart 
and say you release that "ischaemic soup" into a 
haemodynamically stable circulation each and every time?? 
Is this why we get away with it in theatre and not in the 
emergency room? I'm not by any means implying that each 
and every time we take someone to theatre and put a 
tourniquet that we don't have a problem, of course not! 
But it is a no-brainer that a haemodynamically stable 
patient has a better chance...

WHY prophylactic tourniquets are good??
There should be no ambiguity, that circulation 
preservation strategies, i.e. permissive hypotension until 
definitive surgical or interventional radiological 
management of the haemorrhage, takes precedence over any 
crush syndrome protocol. Just thought I'd make that 
statement 1st!  I do believe in the DDIT approach with 
tourniquets as a useful adjunct in the right circumstances 
in haemorrhage control... but may I add once again to the 
argument.... WITH SYSTEMIC PREOPTIMISATION PRIOR TO RELEASE 
!

Do you want a rescuer managing a cardiac arrhythmia during 
the extrication? Do want to manage it in an ambulance? Or 
do you want SOME control over when it is going to occur? 
That is why we teach our rescue personnel to put 
tourniquets on, prior to release and call an appropriately 
qualified person who is able to start a crush protocol to 
go some way to restore systemic normality.

Tourniquets should remain in place until the patient is in 
a safer environment, ideally in a hospital resuscitation 
bay or theatre, with full cardiovascular monitoring, but 
as a sensible compromise, in cases where there is 
potentially a long delay to definitive care or a difficult 
extrication, the stage release protocol could be used 
earlier.

Once in a place of safety, with appropriate monitoring, 
appropriate preoptimisation, a staged release of 
tourniquets is an entirely logical next approach. This is 
currently lacking a clinical effectiveness audit, 
something which I aim to tackle as part of a PhD.

The goal is to do a controlled "infusion" as opposed to 
"bolus" the inevitable ischemic washout. Tourniquets 
should be individually released for a period of thirty 
seconds, whilst monitoring the casualty's condition 
closely and then reapplied for a period of 3 minutes. 
After reapplication, wait for 3 minutes. If the casualty 
is stable, release the other tourniquet (if present) for 
30 seconds. Repeat this procedure with each tourniquet 
being released 3 times until finally being left off. 
During this time a large CO2 and therefore acid load will 
return to the main circulation. Ventilated patients should 
be hyperventilated. Adverse responses can be managed with 
further fluid, pressors, calcium and sodium bicarbonate.

To answer Dr. Mazur's question, there is good evidence in 
support of the early use of potassium binders such as 
sodium polystyrene sulfonate (Sodium or Calcium Resonium) 
orally or rectally before patients are extricated and 
transferred to hospital.[xii] Should Calcium be used 
prophylacticly? Well again, no evidence, but very logical. 
I am looking into the possibility of a study in a 
particularly earthquake prone country... will let the list 
know the results.  But I am about to publish one very good 
case example where we used such agents periarrest in the 
face of massive hyperkalaemia with discharge home 4 days 
later!

I leave you with one thought: It can be argued that we 
have inadvertently been efficiently managing a huge bulk 
of patients at risk of crush syndrome through our 
traditionally liberal approach to fluid resuscitation, 
throughout the trauma patient journey. With today's more 
conservative approach to the use of fluids in trauma, 
could we now begin to see a shift away from such problems 
as fluid overload and ARDS to those of a crush syndrome?

Dr. Jason van der Velde       (EMDM-A, MBChB, BAA)
Disaster Response Coordinator
UN/OCHA Liaison
Anaesthesia Trauma and Critical Care Team
atacc.co.uk

[i] Jonathan Wyatt, Diana Beard, Alasdair Gray, Anthony 
Busuttil, and Colin Robertson. The time of death after 
trauma. BMJ 1995; 310: 1502
[ii] Trunkey DD. Trauma. Sci Am 1983;249(2):20-7
[iii] Sever MS, Erek E, Vanholder R, et al. The Marmara 
earthquake: admission laboratory features of patients with 
nephrological problems. Nephrol Dial Transplant 
2002;17:1025-1031.
[iv] James PB. Cardiac arrest after crush injury. Br Med J 
(Clin Res Ed). 1983 Sep 17;287(6395):839.
[v] Papadopoulos IN, Kanakaris N, Triantafillidis A, et. 
al.  Autopsy findings from 111 deaths in the 1999 Athens 
earthquake as a basis for auditing the emergency response. 
Br J Surg. 2004 Dec;91(12):1633-40
[vi] Frankenthal L. Lieber Verschuettungen. Virchows 
Archives 1916;22:332-45 (in German).
[vii] Apple, F.S., Y. Hellsten, and P.M. Clarkson. Early 
detection of skeletal muscle injury by assay of creatine 
kinase MM isoforms in serum after acute exercise. Clin. 
Chem. 34(6): 1102-1104, 1988.
[viii] Better OS. The crush syndrome revisited 
(1940-1990). Nephron 1990;55:97-103.
[ix] Better OS, Rubinstein I, Reis ND. Muscle crush 
compartment syndrome: fulminant local oedema with 
threatening systemic effects. Kid Int 2003;63:1155-7.
[x] Malinoski DJ, Slater MS, Mullins RJ. Crush injury and 
rhabdomyolysis. Crit Care Clin. 2004 Jan;20(1):171-92
[xi] Gunal AI, Celiker H, Dogukan A, et. al. Early and 
vigorous fluid resuscitation prevents acute renal failure 
in the crush victims of catastrophic earthquakes.  J Am 
Soc Nephrol. 2004 Jul;15(7):1862-7
[xii] Sever MS, Vanholder R, Lameire N. Management of 
crush-related injuries after disasters. N Engl J Med. 2006 
Mar 9;354(10):1052-63.

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