Delayed healing as reason for delaying definitive surgery
MARK FORREST
atacc.doc at btinternet.com
Mon May 26 01:50:13 BST 2008
Dear Ivan
You really do have a big 'issue' with ITU don't you?!
In your world the OR maybe as effective in definitive resuscitation but in the UK we struggle to achieve homeostasis and 'normality' whilst the traumatic insult is continued. In theatre we can certainly commence effective resuscitation but this is rarely if ever completed on the table.
In ITU, not only do we have 'prettier ladies!!!' but also better ventilators, monitors, lung and cardiac assist devices, dialysis, effective whole body warming devices and no disillusioned individual attempting to stop generalised oozing with a knife!
You also completely contradict yourself with your statements about normalisation of cellular metabolism etc followed by the simplistic statement that 'acidosis can be normalised'. This process can take days with a careful balance of filling, inotropes/dilators, re-warming and optimisation of mesenteric, renal and peripheral perfusion. If you can achieve this in theatre in a few hours, during surgery, well you need to tell us all how.
In addition, we envy Ken's team that achieve affective haemostasis so rapidly in theatre, avoiding lengthy surgery, the lethal triad, extended traumatic 'hit' and all the issues of 'staying and playing in theatre'
Sadly in most units in the UK, where Karim and his more dynamic colleagues don't work, the concept of getting into theatre asap, addressing the immediate problem, then getting the hell out before we just make things worse is still something of a theoretical concept rather than standard practice.
As for delayed healing....is that a problem? How many wounds are better left to granulate and close, especially if heavily contaminated at the time of presentation.
Sadly not everything can be cured with a knife in the OR!
Mark F
UK
----- Original Message ----
From: Ivan Hronek <ivanhronek at yahoo.com>
To: trauma-list at trauma.org
Sent: Sunday, 25 May, 2008 11:15:55 PM
Subject: Delayed healing as reason for delaying definitive surgery
Matthew,
I am glad that with your and Karim's help we were able to spell out the reasoning behind the delayed operation/damage control surgery concept.
I think we're agreeing (hope it is not just my bias again) that the reason for delaying definitive surgery is the delayed normalization of cellular metabolism, temperature gradients and inflammatory/coagulation cascade mediator levels.
I believe we were able to exclude acidosis as the reason (as it can be normalized) and the myth that resuscitation in the ITU is "better" (although there occasionally are prettier ladies taking care of the patient there, I admit).
* next is the question how to decrease the perfusion (and temperature) gradients in the body - be adding narcotics and vasodilating the persistently constricted areas (muscles, GI tract, subcutaneous areas) as Rick Dutton once told me ?
* attack the immunoparalysis, prevent calcium influx into impaired cells etc.
________________________________
________________________________
Immunoparalysis and Adverse Outcomes from Critical Illness
Pediatric Clinics of North America - Volume 55, Issue 3 (June 2008)The clinical significance of immunoparalysis
http://www.mdconsult.com/das/article/body/95678832-3/jorg=clinics&source=&sp=20696840&sid=708942888/N/645223/1.html?issn=0031-3955
excerpt:
Trauma
Trauma surgeons were among the first clinicians to study the innate immune response in the setting of critical illness. In 1986, Polk and colleagues [16]undertook a systematic evaluation of 20 adults who had severe trauma. The results of their analyses indicated that persistently impaired monocyte antigen-presenting capacity was associated with development of nosocomial sepsis. All of the traumatized patients had reduced monocyte HLA-DR expression compared with healthy controls when first evaluated on ICU admission. It was those who exhibited prolonged HLA-DR down-regulation in whom secondary sepsis developed more often. These findings were confirmed by Livingston and colleagues [18]in a separate series of adult trauma patients. It seems that the initial reduction in monocyte HLA-DR expression is indicative of the CARS state and not itself pathologic. Rather, it is the failure of HLA-DR expression to recover to normal levels over time that places
patients at risk for developing nosocomial sepsis.
The ability of HLA-DR expression profile to predict outcome in traumatized adults was strengthened by the work of Cheadle and colleagues [60]in 1989 in a study of serial monocyte HLA-DR measurements in 60 trauma victims beginning the first 24 hours after injury. In their cohort, the depth and persistence of HLA-DR expression was predictive of development of secondary infection. The study differed from previous work in that monocytes with low HLA-DR expression underwent ex vivo LPS-induced stimulation. Patients who developed secondary sepsis but went on to survive had low initial monocyte HLA-DR expression that was reversible by LPS stimulation. In contrast, persistently low HLA-DR expression, even after ex vivo LPS stimulation, was characteristic of patients who died.
Ex vivo TNF-ɑ production also is correlated with outcome in clinical trauma studies. Majetschak and colleagues [28]in 1999 performed ex vivo LPS-induced stimulation of whole blood samples from 46 adult blunt trauma victims. They documented a profound reduction in patients' TNF-ɑ production compared with healthy controls. The degree of reduction in the TNF-ɑ response was associated with the severity of injury and this reduction was detectable in samples obtained within 90 minutes after trauma.Patients requiring surgery to treat their injuries experienced a further impairment in their TNF-ɑ response.
________________________________
________________________________
Increased vagal tone accounts for the observed immune paralysis in patients with traumatic brain injury
http://www.mdconsult.com/das/article/body/95678832-3/jorg=journal&source=MI&sp=20406500&sid=708942891/N/628630/1.html?issn=0028-3878
Neurology - Volume 70, Issue 6 (February 2008)
ABSTRACT
Traumatic brain injury (TBI) is a leading cause of death and disability, especially in the younger population. In the acute phase after TBI, patients are more vulnerable to infection, associated with a decreased immune response in vitro. The cause of this immune paralysis is poorly understood. Apart from other neurologic dysfunction, TBI also results in an increase in vagal activity. Recently, the vagus nerve has been demonstrated to exert an anti-inflammatory effect, termed the cholinergic anti-inflammatory pathway. The anti-inflammatory effects of the vagus nerve are mediated by the ɑ7 nicotinic acetylcholine receptor present on macrophages and other cytokine-producing cells. From these observations, we hypothesize that the immune paralysis observed in patients with TBI may, at least in part, result from augmented vagal activity and subsequent sustained effects of the cholinergic anti-inflammatory pathway. This pathway may counteract systemic
proinflammation caused by the release of endogenous compounds termed alarmins as a result of tissue trauma. However, sustained activity of this pathway may severely impair the body's ability to combat infection. Since the cholinergic anti-inflammatory pathway can be pharmacologically modulated in humans, it could represent a novel approach to prevent infections in patients with TBI.
Mechanisms and innovations Traumatic brain injury: Can the consequences be stopped?
Canadian Medical Association Journal - Volume 178, Issue 9 (April 2008) Key points
• Severe traumatic brain injury is a leading cause of morbidity and mortality worldwide.
• Abnormal intracellular calcium homeostasis is a central feature of both grey and white matter secondary injury.
• White matter injury is important in the prognosis of both severe and mild injury.
• Recent studies point to trauma-induced changes in neuronal receptor composition that render cells vulnerable to delayed injury.
Box 1. Glossary of terms
αII-spectrin: A structural protein involved in the maintenance of axonal shape. A key target of calpains after trauma.
AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid): Chemical agonist selective for the AMPA class of excitatory glutamate receptors.
Ionic homeostasis: The naturally occurring gradient of intracellular ion concentrations within a cell.
β-amyloid precursor protein: A protein transported by axons. It can be used as an immunohistochemical marker of axonal injury. This protein accumulates in injured axons with impaired transport and contributes to axonal swelling.
Calpains:A family of enzymes that degrade numerous intracellular proteins. Calpains are activated by high levels of intracellular calcium.
Caspase-3:A calcium-activated enzyme referred to as the “executioner caspase” because of its role in initiating programmed cell death.
Cytoskeleton:Proteins that comprise the cell’s structural “skeleton.”
Excitoxicity:Over-activation of glutamate receptors leads to a massive sodium and calcium influx that results in rapid cell death.
GluR2: The AMPA-receptor subunit that determines whether the receptor is permeable to calcium. AMPA receptors that include the GluR2 subunit are not permeable to calcium.
Immunohistochemistry: A technique used to visually identify specific proteins in tissues by use of antibodies against specific antigens.
NMDA (N-methyl-D-aspartic acid): Chemical agonist selective for the NMDA class of glutamate receptors
Primary cell culture: A laboratory technique of growing cells on a plate. Primary cell culture is often used for in vitro experiments.
Reactive astrocytosis: A characteristic response of astrocytes (subtype of glial cells) to injuries of the central nervous system. It includes proliferation and processes extension, and it can be visualized by histological examination of increased expression of an astrocyte marker (glial fibrillary aidic protein).
Secondary axotomy: The process by which axons become disconnected after a delay following initial trauma. Occurs as the result of subcellular events not the force of the initial injury.
Superoxide, peroxynitrite, nitric oxide: Reactive oxygen species that can contribute to the destruction of cell membranes and DNA breakdown leading to cell death.
Traumatic axonal injury: The delayed and progressive deterioration of white matter following trauma.
Tumour necrosis factor α:A cytokine secreted by inflammatory cells that is capable of initiating cell-death pathways as well as modulating glutamate-receptor composition.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1384607
http://www.galenicom.com/zh/medline/article/18048039/Immunoparalysis+after+multiple+trauma.
http://content.karger.com/ProdukteDB/produkte.asp?Aktion=ShowFulltext&ArtikelNr=18755&Ausgabe=225615&ProduktNr=223996
Ivan Hronek MD
SFMC, Los Angeles, CA Do not fear to be eccentric in opinion, for every opinion now
accepted was once eccentric. - Bertrand Russell-
________________________________
Confidentiality Notice: This transmission and any attached documents may be confidential and contain information protected by State and Federal Medical Privacy statutes and is legally privileged. They are intended for use only by the addressee. If you are not the intended recipient of this transmission, or an agent of the intended recipient, you are prohibited from reading, disclosing, printing, saving, copying, using, or otherwise disseminating any information contained in this transmission. If you received this transmission in error, please accept our apologies and notify me at ivanhronek at yahoo.comand delete the entire message and its attachments. Thank you. Disclaimer: this message contains the personal views of the author. The author will not be responsible in any way for procedures or approaches perfomed in the way suggested in this note.
________________________________
----- Original Message ----
From: Matthew Reeds <mgreeds at reeds.uk.com>
To: "Trauma & Critical Care mailing list" <trauma-list at trauma.org>
Sent: Sunday, May 25, 2008 5:11:09 AM
Subject: Turning of(f) the tap!
I believe that this is part of the common misconception that many have. The
lethal triad is an extremely important first step at highlighting the
problems encountered - but that is all. To assume that if you warm the
patient up/operate in a hot environment, give large amounts of clotting
factors and have a "normal" base excess/pH on the blood gas and/or give
bicarbonate means that you have corrected the problem - you do not truly
understand the problem and the underlying physiology of the patient.
Appreciating that inflammation has a significant impact upon coagulation,
the lethal triad does not address the profound release of interleukins,
cytokines, leukotrienes, bradykinin, complement (especially C3), histamine,
platelet derived growth factor, tumour necrosis factor, arachidonic acid
etc. etc. etc. that affects the patient (and that is an extremely simplified
basic version) and so the list goes on.. It is addressing these problems
that will correct the underling deleterious pathophysiology which is
occurring but this is clearly easier said than done!!
The innate physiological response of the body has a pro-inflammatory and an
anti-inflammatory mechanism which act interchangeably with one another. Too
much of one and the patient suffers harmful effects and the body either
cannot defend itself and fight off infection (i.e. synonymous with an
immune-deficient state) or the immune response is profoundly overwhelming
for the body's immune system to cope with it.
It is when these extreme problems at a cellular level have been addressed or
(at the very least) limited, that further DCS or definitive operative
intervention can continue without the profound adverse effects affecting the
patient which would otherwise result.
Matthew
-----Original Message-----
From: Karim Brohi [mailto:karimbrohi at gmail.com]
Sent: 24 May 2008 12:21
To: Trauma &, Critical Care mailing list
Subject: Re: Turning of(f) the tap!
Ivan, it's important to remember that coagulopathy, acidaemia and
hypothermia are not the problem. They are markers of underlying
disturbances in tissue perfusion and activation of inflammation (by which I
especially imply innate immunity including the endothelium, complement, the
inflammatory component of what we understand as 'coagulation' and the innate
cellular response). As an example, hypothermia doesn't exist because the
room is cold, but because of reduced muscle perfusion, mitochondrial
dysfunction etc etc. (Hence the important difference between acquired
hypothermia and induced hypothermia). Similarly acidaemia is a crude,
global marker for the massive systemic changes that are going on in cellular
function.
Merely giving bicarbonate or THAM is like cutting interest rates to solve
the credit crunch!!! It fiddles at the edges without in anyway acting on
the underlying (deeper and more complicated) causes, and may indeed lead to
unintended consequences that exacerbate the situation. But it makes
everyone feel better.
So when we say, 'this patient's physiology is normal because they're not
acidotic, clotting normally and normovolaemic, what we're really saying is
that cellular perfusion and functions are normalising , and that there is no
further ischaemic activation of inflammation and no further reperfusion
events are expected. So further operative trauma is unlikely to severely
exacerbate the status of the inflammatory systema and if you go ahead and
re-anastomose two piece of bowel, chances are that they'll stay stuck
together!
Karim
On Sat, May 24, 2008 at 4:40 AM, Ivan Hronek <ivanhronek at yahoo.com> wrote:
> Karim,
>
> Hope I'm not confirming my bias now if I say that I agree that acidosis
> persists despite sufficient resuscitation for a while. Other indices of
> homeostasis can I believe be taken care of.
> I do not really think that open body cavities are an issue as temperature
> is not usually a problem - at least not here in Southern California - and
a
> little crystalloid will easily replace the evaporative and other fluid
> losses.
>
> So is it just because of the persisting acidosis that we pack up asap and
> go to the ITU - is that the reason why more patients survive ? Is it just
> because of decreased coagulation problems ? Even if we normalize the pH
with
> NaHCO3 or THAM ?
> Ivan Hronek
> MD
> SFMC, Los Angeles, CA Do
not
> fear to be eccentric in opinion, for every opinion now
> accepted was once eccentric. - Bertrand Russell-
> ________________________________
>
> Confidentiality Notice: This transmission and any attached documents may
be
> confidential and contain information protected by State and Federal
Medical
> Privacy statutes and is legally privileged. They are intended for use only
> by the addressee. If you are not the intended recipient of this
> transmission, or an agent of the intended recipient, you are prohibited
from
> reading, disclosing, printing, saving, copying, using, or otherwise
> disseminating any information contained in this transmission. If you
> received this transmission in error, please accept our apologies and
notify
> me at ivanhronek at yahoo.comand delete the entire message and its
> attachments. Thank you. Disclaimer: this message contains the personal
views
> of the author. The author will not be responsible in any way for
procedures
> or approaches perfomed in the way suggested in this note.
> ________________________________
>
>
>
>
> ----- Original Message ----
> From: Karim Brohi <karimbrohi at gmail.com>
> To: "Trauma &, Critical Care mailing list" <trauma-list at trauma.org>
> Sent: Friday, May 23, 2008 2:48:27 PM
> Subject: Re: Turning of(f) the tap!
>
> Ivan,
>
> I think you read my message to confirm your own bias. I do not have a
> stance on OR resuscitation being better than current damage control
> practice
> of ICU resuscitation. At the moment this is the best we have.
>
> The problem currently is that for the **actively bleeding** patient,
> current
> resuscitation capabilities can only do so much. Over resuscitation during
> active haemorrhage makes things worse (much worse). We are unable to
> maintain homeostasis during this acute period. Further, once haemorrhage
> has stopped in may take some hours to restore normal physiology to these
> patients. Trying to do it with open cavities is much harder and takes much
> longer. It is a bad use of OR time to have a patient sit there for hours
> waiting to normalise physiology, so they go to ICU and come back.
>
> I can envision a time when we have directed interventions to avoid this
> loss
> of homeostasis. But we're nowhere near there yet and damage control with
> staged operations is the current gold standard.
>
> Karim
>
> On Fri, May 23, 2008 at 2:25 PM, Ivan Hronek <ivanhronek at yahoo.com> wrote:
>
> > Karim,
> >
> > I fully agree with your stance on OR resuscitation: I am going to be
> iconoc
> > lastic again and will maintain alongside with you that it is a fallacy
> that
> > ITU resuscitation is better than OR resuscitation.
> > It fits in the 'damage control' surgery approach, which may be OK;
> however
> > we should not be fooling ourselves and say it is a good approach because
> of
> > ITU resuscitation being better than OR resuscitation.
> > Is the damage control approach so much better for other reasons then ?
> What
> > are those reasons ?
> > Ivan Hronek
> > MD
> > SFMC, Los Angeles, CA Do
> not
> > fear to be eccentric in opinion, for every opinion now
> > accepted was once eccentric. - Bertrand Russell-
> > ________________________________
> >
> > Confidentiality Notice: This transmission and any attached documents may
> be
> > confidential and contain information protected by State and Federal
> Medical
> > Privacy statutes and is legally privileged. They are intended for use
> only
> > by the addressee. If you are not the intended recipient of this
> > transmission, or an agent of the intended recipient, you are prohibited
> from
> > reading, disclosing, printing, saving, copying, using, or otherwise
> > disseminating any information contained in this transmission. If you
> > received this transmission in error, please accept our apologies and
> notify
> > me at ivanhronek at yahoo.comand delete the entire message and its
> > attachments. Thank you. Disclaimer: this message contains the personal
> views
> > of the author. The author will not be responsible in any way for
> procedures
> > or approaches perfomed in the way suggested in this note.
> > ________________________________
> >
> >
> >
> >
> > ----- Original Message ----
> > From: Karim Brohi <karim at trauma.org>
> > To: "Trauma &, Critical Care mailing list" <trauma-list at trauma.org>
> > Sent: Tuesday, May 20, 2008 2:13:06 AM
> > Subject: Re: Turning of(f) the tap!
> >
> > Mark:
> >
> > Do we really know the things we think we definitely know?
> >
> > So can the list members consider what is accepted or agreed ? What we do
> > > know?
> > > - your own blood is the best fluid in your vessels?
> >
> >
> > Initially yes. Afterwards perhaps not. If you believe in 1:1, then
> whole
> > blood is only 1:2. Also your own blood is almost certainly better than
> > someone elses, due to its immunogenicity. There may also be real
> > activation
> > of inflammatory factors in shed blood.???
> >
> > >
> > > - hypothermia is a greatly under-estimated problem and must be
> > aggressively
> > > avoided
> >
> >
> > Unless its induced hypothermia in which case it may be life saving????
> >
> > >
> > > -Damage control surgery is a good thing
> >
> >
> > At the moment - but if we could get better at maintaining homeostasis,
> > would
> > we still recommend it. Will we still be doing damage control in 10
years
> > time?
> >
> >
> > >
> > > -Haemoglobin of 7-8g/dl is an acceptable target for transfusion
> >
> >
> > ICU studies would say 6. Is it the same if you're in shock and actively
> > bleeding?
> >
> > -Excessive crystalloid or colloid is not good - 'cyclic
hypersuscitation'
> >
> >
> > Can't argue with this one - except that it's not just cyclic
> > hyperresuscitation and that excessive any fluid is probably bad
> >
> > >
> > > -ITU is the place for defintive resuscitation after damage control
> >
> >
> > Again. Shouldn't we be getting better at maintaining homestasis in the
> OR?
> > If you could close temporarily and correct physiology in the OR perhaps
> you
> > could reopen after 30 minutes or so and complete????
> >
> > >
> > > - Once you have a significant coagulopathy you have 'missed the boat'?
> >
> >
> > Well since 1 in 4 patients arrive with a coagulopathy this would be bad.
> > We
> > need to find an optimal way of getting the boat to turn back and pick
> them
> > up. Especially if we can unravel the mechanism of this coagulopathy and
> > develop inhibitors to it (rather than our current strategy of pouring in
> > more and more clotting factors)
> >
> > >
> > >
> > > I am sure that we could all come up with a reliable and agreed
> > list...dare
> > > I say 'proven'!
> >
> >
> > Ever the optimist!!!
> >
> > Karim
> >
> >
> --
> trauma-list : TRAUMA.ORG
> To change your settings or unsubscribe visit:
> http://www.trauma.org/index.php?/community/
>
>
>
>
> --
> trauma-list : TRAUMA.ORG
> To change your settings or unsubscribe visit:
> http://www.trauma.org/index.php?/community/
--
trauma-list : TRAUMA.ORG
To change your settings or unsubscribe visit:
http://www.trauma.org/index.php?/community/
________________________________
________________________________
________________________________
--
trauma-list : TRAUMA.ORG
To change your settings or unsubscribe visit:
http://www.trauma.org/index.php?/community/
More information about the trauma-list
mailing list