Delayed healing as reason for delaying definitive surgery

[Sise, Mike MD]

Jose,
 
You have pointed to a very significant problem that we all face - too much focus on the blood pressure and not enough on the overall state of hemostasis and perfusion. If a patient is bleeding from torso or orthopedic injuries and has a head injury, the steps that yield prompt control of bleeding without deleterious hemodilution and pro-inflammatory effects are much more important than a short-term focus on cerebral perfusion pressure. I suspect that the studies of permissive hypotension being done at the Ben Taub and other centers will show that brain injured patients do better overall by stopping the bleeding first then focusing on cerebral perfusion pressure. 
 
But this remains speculation and we need good data from thoughtfully studied series of patients to draw the conclusions that support improved practice guidelines. Let's hope we get that data soon.
 
Mike Sise
San Diego

________________________________

From: josemaya01 [mailto:josemaya01 at prodigy.net.mx]
Sent: Tue 5/27/2008 11:21 AM
To: trauma-list
Subject: Ref:RE: Delayed healing as reason for delaying definitive surgery



The problem is that we cannot handle all trauma patients the same, there will always be different subgroups of patients that will require different approaches according to their needs. TBI is such a subgroup of patients in which the philosophy of 1:1:1 would have to be rethought and a BP of 90 should be aimed for.

José Mayagoitia MD
Hosptial General de Mexicali
Mexicali, México


De : "Anthony Caruso" medic541 at hotmail.com
Para : "Trauma & Critical Care mailing list" trauma-list at trauma.org
Copia :
Fecha : Mon, 26 May 2008 14:52:53 -0400
Asunto : RE: Delayed healing as reason for delaying definitive surgery


>
>
> Mike, interesting to say the least. I have a question however. I have done a bit of reading on this, as well as have seen it on this list from time to time. What do you do if the pressure drops below 90 systolic with a head injured patient? I believe that if a pressure drops below 90 systolic that the patient has a 60% chance of the injury to be fatal. (Keeping in mind that the near hypotension is related to blood loss and not necessarily a neurogenic issue). Do we infuse crystalloid's to keep the presure up? We have discussed on this list that infusing a large amount of crystalloids has a worse outcome than holding off on giving them. I suppose this would be a question for one in the pre hospital arena as well as in the EW. Any thoughts?
>
> Anthony M. Caruso EMT-P
>
> 'God Bless our troops this memorial day"
>
>
> Date: Mon, 26 May 2008 06:13:47 -0700From: Sise.Mike at scrippshealth.orgTo: trauma-list at trauma.orgSubject: RE: Delayed healing as reason for delaying definitive surgery
>
>
> Mark,
>
> Any maneuver, infusion of fluid or blood, application of any external device, external heating, or medication administered to someone who is bleeding or will bleed again if the blood pressure is increased probably should only be used as a bridge step to getting control of the bleeding source and stopping it. If that means getting to the operating room or interventional radiology suite ASAP - then go there. Any other venue of care is very likely to lead to delays in definitive care for bleeding patients. If the above mentioned steps are required to keep the patient alive while getting to the operating room or radiology suite - they are appropriate. It is very revealing to take this approach and realize that elevating the blood pressure in the Emergency Center or Trauma Room was, in fact, a goal we all pursued without realizing that it needlessly increased bleeding and worsened the physiologic "hit".
>
> In the early 80's in the US we had the same problem you cite in the UK. In most communities we had trouble getting bleeding patients to the operating room with the right surgeon. All around the US, surgeons and emergency medicine physicians spoke up and demanded organized trauma systems. 20 years later we have these systems with reproducible results. I can only encourage you and your colleagues to speak out early and often.
>
> Mike Sise
>
>
> From: MARK FORREST [mailto:atacc.doc at btinternet.com]Sent: Sun 5/25/2008 5:50 PMTo: Trauma & Critical Care mailing listSubject: Re: Delayed healing as reason for delaying definitive surgery
>
> Dear IvanYou 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 FUK----- Original Message ----From: Ivan Hronek To: trauma-list at trauma.orgSent: Sunday, 25 May, 2008 11:15:55 PMSubject: Delayed healing as reason for delaying definitive surgeryMatthew,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 IllnessPediatric Clinics of North America - Volume 55, Issue 3 (June 2008)The clinical significance of immunoparalysishttp://www.mdconsult.com/das/article/body/95678832-3/jorg=clinics&source=&sp=20696840&sid=708942888/N/645223/1.html?issn=0031-3955excerpt:TraumaTrauma 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 placespatients 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-? 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-? production compared with healthy controls. The degree of reduction in the TNF-? 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-? response.________________________________________________________________Increased vagal tone accounts for the observed immune paralysis in patients with traumatic brain injuryhttp://www.mdconsult.com/das/article/body/95678832-3/jorg=journal&source=MI&sp=20406500&sid=708942891/N/628630/1.html?issn=0028-3878Neurology - 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 ?7 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 systemicproinflammation 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 pointso Severe traumatic brain injury is a leading cause of morbidity and mortality worldwide.o Abnormal intracellular calcium homeostasis is a central feature of both grey and white matter secondary injury.o White matter injury is important in the prognosis of both severe and mild injury.o Recent studies point to trauma-induced changes in neuronal receptor composition that render cells vulnerable to delayed injury.Box 1. Glossary of terms?II-spectrin: A structural protein involved in the maintenance of axonal shape. A key target of calpains after trauma.AMPA (?-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.?-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 receptorsPrimary 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 ?: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=1384607http://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 nowaccepted 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 To: "Trauma & Critical Care mailing list" Sent: Sunday, May 25, 2008 5:11:09 AMSubject: Turning of(f) the tap!I believe that this is part of the common misconception that many have. Thelethal triad is an extremely important first step at highlighting theproblems encountered - but that is all. To assume that if you warm thepatient up/operate in a hot environment, give large amounts of clottingfactors and have a "normal" base excess/pH on the blood gas and/or givebicarbonate means that you have corrected the problem - you do not trulyunderstand 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 acidetc. etc. etc. that affects the patient (and that is an extremely simplifiedbasic version) and so the list goes on.. It is addressing these problemsthat will correct the underling deleterious pathophysiology which isoccurring but this is clearly easier said than done!!The innate physiological response of the body has a pro-inflammatory and ananti-inflammatory mechanism which act interchangeably with one another. Toomuch of one and the patient suffers harmful effects and the body eithercannot defend itself and fight off infection (i.e. synonymous with animmune-deficient state) or the immune response is profoundly overwhelmingfor 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 operativeintervention can continue without the profound adverse effects affecting thepatient which would otherwise result.Matthew-----Original Message-----From: Karim Brohi [mailto:karimbrohi at gmail.com]Sent: 24 May 2008 12:21To: Trauma &, Critical Care mailing listSubject: Re: Turning of(f) the tap!Ivan, it's important to remember that coagulopathy, acidaemia andhypothermia are not the problem. They are markers of underlyingdisturbances in tissue perfusion and activation of inflammation (by which Iespecially imply innate immunity including the endothelium, complement, theinflammatory component of what we understand as 'coagulation' and the innatecellular response). As an example, hypothermia doesn't exist because theroom is cold, but because of reduced muscle perfusion, mitochondrialdysfunction etc etc. (Hence the important difference between acquiredhypothermia and induced hypothermia). Similarly acidaemia is a crude,global marker for the massive systemic changes that are going on in cellularfunction.Merely giving bicarbonate or THAM is like cutting interest rates to solvethe credit crunch!!! It fiddles at the edges without in anyway acting onthe underlying (deeper and more complicated) causes, and may indeed lead tounintended consequences that exacerbate the situation. But it makeseveryone feel better.So when we say, 'this patient's physiology is normal because they're notacidotic, clotting normally and normovolaemic, what we're really saying isthat cellular perfusion and functions are normalising , and that there is nofurther ischaemic activation of inflammation and no further reperfusionevents are expected. So further operative trauma is unlikely to severelyexacerbate the status of the inflammatory systema and if you go ahead andre-anastomose two piece of bowel, chances are that they'll stay stucktogether!KarimOn Sat, May 24, 2008 at 4:40 AM, Ivan Hronek 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 - anda> 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 pHwith> NaHCO3 or THAM ?> Ivan Hronek> MD> SFMC, Los Angeles, CA Donot> fear to be eccentric in opinion, for every opinion now> accepted was once eccentric. - Bertrand Russell-> ________________________________>> Confidentiality Notice: This transmission and any attached documents maybe> confidential and contain information protected by State and FederalMedical> 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 prohibitedfrom> 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 andnotify> me at ivanhronek at yahoo.comand delete the entire message and its> attachments. Thank you. Disclaimer: this message contains the personalviews> of the author. The author will not be responsible in any way forprocedures> or approaches perfomed in the way suggested in this note.> ________________________________>>>>> ----- Original Message ----> From: Karim Brohi > To: "Trauma &, Critical Care mailing list" > 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 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 > > To: "Trauma &, Critical Care mailing list" > > 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 10years> > 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 - 'cyclichypersuscitation'> >> >> > 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.ORGTo change your settings or unsubscribe visit:http://www.trauma.org/index.php?/community/________________________________________________________________________________________________--trauma-list : TRAUMA.ORGTo change your settings or unsubscribe visit:http://www.trauma.org/index.php?/community/
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