Sum:Ketamine & Etomidate Indic. & Contraindications

[IVAN HRONEK]

Head trauma - avoid Ketamine, although perhaps OK to to increase CPP, if not achieveable otherwise and herniation not pending (neurol change, unilateral blown pupil)
 
Trauma without head trauma-  Etomidate OK, Ketamine OK unless catecholamines depleted or very tachycardic
Sepsis - avoid EtomidateIvan Hronek MDChief, Critical Care & Trauma AnesthesiaSFMC Gas, Inc.St. Francis Medical Center3630 E. Imperial HighwayLynwood, CA 90262 Cell: 310 487-3288Pager: 310 636-6020

> Date: Thu, 2 Aug 2007 17:59:10 +0200> From: markus.weis at med.lu.se> To: trauma-list at trauma.org> Subject: Re: ***SPAM*** Etomidate & adrenal suppress. - OK to use-may add steroids> > Here you go Ivan.> > The attached editorial (and the response) is one of many articles that I> came across whilst learning more about an induction agent that is not an> approved drug (and I don't know if it has ever been) where I work.> > Markus> > > On 8/2/07, IVAN HRONEK <ih7 at msn.com> wrote:> >> > Markus,> >> > it's hard to know what they are talking about in the papers you listed,> > MDconsult lists only citations. Can you mail the actual articles or> > abstracts so we'd know what we are talking about ?> > I do believe in many situations there is no replacement for Etomidate and> > we use it like water - and here's my reasons:> >> >> >> >> >> >> > Adrenocortical dysfunction following etomidate induction in emergency> > department patients. - Schenarts CL - Acad Emerg Med - 01-JAN-2001; 8(1):> > 1-7 (From NIH/NLM MEDLINE)> >> > OBJECTIVE: To assess adrenocortical function following intravenous> > etomidate use in emergency department (ED) patients requiring intubation.> > METHODS: This was a prospective, randomized, controlled trial of consecutive> > patients presenting to the ED requiring intubation. Patients were randomized> > to receive a single bolus induction dose of either 0.05-0.1 mg/kg> > midazolam (control group) or 0.3 mg/kg etomidate (etomidate group) during> > a standardized rapid-sequence intubation (RSI) with succinylcholine. The> > primary outcome variable was adrenocortical function at 4, 12, and 24 hours> > post-induction as assessed by measured serum cortisol response to exogenous> > cosyntropin (cosyntropin stimulation test, CST). Fisher's exact test was> > used to compare CST results between groups. RESULTS: Thirty-one patients> > were enrolled: 8 control, 10 etomidate, and 13 excluded from analysis for> > either incomplete data or steroid use during the study period. The 4-hour> > CST results were significantly diffe> > rent between study groups, with a normal response in 100% of control> > patients vs 30% of etomidate patients (p = 0.004). The 12- and 24-hour> > CSTs did not differ significantly between groups: normal CST in 100% of> > control patients at 12 and 24 hours vs 100% and 90% among etomidate patients> > at 12 and 24 hours, respectively (p = 1.0 at 12 and 24 hours). Measured> > cortisol levels of patients with abnormal CSTs remained within normal> > laboratory reference ranges. CONCLUSION: Use of etomidate in ED patients> > requiring RSI results in adrenocortical dysfunction. However, cortisol> > levels remain within normal laboratory levels during this period of> > dysfunction. Adrenocortical dysfunction appears to resolve within 12 hours> > of a single bolus dose of 0.3 mg/kg> > etomidate.> >> > Should etomidate be the induction agent of choice for rapid sequence> > intubation in the emergency department?Oglesby AJ - Emerg Med J -> > 01-NOV-2004; 21(6): 655-9> >> > The ideal induction agent for emergency airway management should be> > rapidly acting, permit optimum intubating conditions, and be devoid of> > significant side effects. This review was performed to ascertain whether> > etomidate should be the induction agent of choice for rapid sequence> > intubation (RSI) in the emergency department, specifically examining its> > pharmacology, haemodynamic profile, and adrenocortical effects. A search of> > Medline (1966-2002), Embase (1980-2002), the Cochrane controlled trials> > register, and CINAHL was performed. In addition, the major emergency> > medicine and anaesthesia journals were hand searched for relevant material.> > Altogether 144 papers were identified of which 16 were relevant. Most> > studies were observational studies or retrospective reviews with only one> > double blind randomised controlled trial and one un-blinded randomised> > controlled trial. Appraisal of the available evidence suggests that> > etomidate is an effective induction agent for emergency depa> > rtment RSI; it has a rapid onset of anaesthesia and results in> > haemodynamic stability, even in hypovolaemic patients or those with limited> > cardiac reserve. Important questions regarding the medium to long term> > effects on adrenocortical function (even after a single dose) remain> > unanswered.> >> >> >> >> >> >> >> > Etomidate for Endotracheal Intubation in Sepsis> > Chest - Volume 127, Issue 3 (March 2005) - Copyright (c) 2005 The American> > College of Chest Physicians - About This Journal> >> >> >> > Editorials> >> >> > Etomidate for Endotracheal Intubation in Sepsis> > Acknowledging the Good While Accepting the Bad> > We would like to commend Dr. Jackson (see page 1031) on both his> > historical review and critical appraisal of the use of etomidate as an> > anesthetic induction agent. This appraisal is a good summary of the debate> > that has occurred over the past quarter century in regard to the safety of> > etomidate as an anesthetic induction agent. The observations of Led ingham> > and Watt[1] in the early 1980s indicated that etomidate should not be used> > for long-term sedation in the ICU due to the mortality cost incurred from> > long-term adrenal suppression. The effect of etomidate on adrenal function> > is both dose-dependent and cumulative. A single dose of etomidate will blunt> > the adrenocortical axis for up to 24 h. The effect of short-term suppression> > of adrenal synthesis on patient outcome is, however, less clear. This> > clinical question, although seemingly simple, is quite complex. The net> > effect of etomidate as an anesthetic induction agent is the sum of several> > factors. Etomidate has several pro> > perties, which makes it, at least in theory, a good first-line anesthetic> > induction agent. The dose required to achieve unconsciousness is relatively> > predictable. This hypnotic effect is much more predictable than that with> > benzodiazepines. The onset of action is fast, essentially in one arm to> > brain circulation. In addition, etomidate has a short duration of action.> > Etomidate does not cause histamine release, which is a factor contributing> > to its relative hemodynamic stability (the reader is referred to an in-depth> > clinical review of the pharmacology of etomidate[2] ). One would expect that> > these factors would result in a mortality benefit; however, the magnitude of> > this benefit is unknown. The major concern regarding the use of etomidate is> > transient adrenal suppression. The unpublished subgroup analysis data> > presented in the study by Annane et al[3] may provide us with a glimpse of> > the cost resulting from the adrenal suppression by etomidate. The fact that> > 68 of the 72 pa> > tients (94%) who received etomidate for the induction of anesthesia did> > not respond to a high-dose cosyntropin stimulation test, is consistent with> > other published reports of adrenal insufficiency 12 to 24 h after the> > administration of etomidate. The data from the study by Annane et al[3]> > seems to indicate a significant mortality cost for etomidate anesthetic> > induction in septic patients. The mortality rate in the placebo-treated> > group was 75.7% vs 54.8% for the corticosteroid-treated group. These data> > indicate that the adrenal insufficiency of sepsis should be treated with the> > administration of stress doses of corticosteroids. The continued use of> > etomidate for anesthesia induction would be a clinical conundrum if this> > mortality effect persisted despite corticosteroid administration. From the> > available data, we have a presumed, but have not yet measured, mortality> > benefit incurred from the beneficial effects of etomidate as an anesthetic> > induction agent. The mortality cost> > of adrenal suppression by etomidate anesthesia induction seems to be> > completely offset by corticosteroid administration in those patients who> > show evidence of adrenal insufficiency. As a result, we feel that the net> > effect still favors the use of etomidate as an anesthesia induction agent.> > The choice of induction agent in hemodynamically labile septic patients is> > inherently complex, as no perfect anesthesia induction agent exists.> > Midazolam is typically underdosed when used as the sole anesthetic induction> > agent, and the time to peak effect is unpredictable.[4] Propofol and> > barbiturate induction delivers rapid, predictable unconsciousness, with> > equally predictable hypotension. Ketamine is perhaps the only available> > agent that provides equally favorable sedation and hemodynamic qualities as> > those of etomidate, but with its own set of adverse reactions. Dr. Jackson> > suggests that the induction of unconsciousness and adequate muscular> > relaxation are measures of the utility of an anesthetic induction agent. We> > would like to reinforce the notion that these are different issues. Firstly,> > look at intubation success, and the optimal laryngeal view is best> > facilitated by muscular relaxation in the form of paralysis. Achieving this> > level of relaxation with most anesthetic> > induction agents will only further worsen hypotension during intubation.> > Furthermore, many of these patients should be considered to have full> > stomachs, and a rapid-sequence intubation with both an anesthetic induction> > agent and a paralytic agent should limit the risk of aspiration.> > Sepsis continues to be a high-mortality illness. Optimal treatment> > requires attention to detail and the implementation of many time-dependent> > therapies starting at the recognition of occult sepsis. We should strive for> > early empiric antibiotic administration. Early goal-directed resuscitation,> > as proposed by Rivers et al,[5] has been shown to reduce mortality in this> > patient population. The treatment of sepsis-induced adrenal insufficiency> > and tight glycemic control play a significant role in reducing mortality.> > High-risk patients benefit from the administration of activated protein C.> > The treatment of sepsis at this time is akin to our current understanding of> > acute myocardial infarction. There is no magic bullet; rather, several> > therapies must be quickly brought to bear on this complex pathologic state> > to maximize the benefit of each intervention while limiting the incurred> > risk. In our minds, the same holds true for the intubation of a septic> > patient. This is a high-stakes> > intervention with a large potential cost if it is not performed well.> > Significant aspiration or a prolonged period of hypotension may well abolish> > any benefit from all of the above therapies. We think that etomidate is> > still a very good agent for the induction of unconsciousness, and when> > combined with muscle relaxation provides the best scenario for rapid,> > smooth, hemodynamically stable intubation. The ba sics of care, the "ABCs,"> > should not be forgotten. Immediate correction of respiratory failure should> > be performed in a manner that impacts the circulatory system the least. In a> > Dutch study, Arbous et al[6] demonstrated that about two thirds of the> > mortality during the induction phase of anesthesia was due to cardiovascular> > events. This underscores the need for hemodynamic stability during> > anesthesia induction. Etomidate provides the stability and predictability> > needed to be a first-line agent. From a practical standpoint, a better> > anesthetic induction agent is simply no> > t available. As Jackson states it, it is sometimes necessary to stabilize> > the immediate situation while accepting a future cost. In this case, the> > future cost is adrenal suppression. Fortunately, the limited available data> > indicate that this effect is completely reversed with the administration of> > corticosteroids. For this reason, we think that all hypotensive septic> > patients should be treated with stress doses of corticosteroids,> > particularly if the random (stress) cortisol level is < 25 μg/dL.[7] We> > recommend initiating therapy with hydrocortisone, 100 mg IV every 8 h, until> > the results of the stress cortisol level measurements are available. The> > "cost" of such an approach is likely to be very low, and the potential> > benefit to be quite high. The cost of such an approach is likely to be very> > low, and the potential benefit to be quite high.> > Dr. Murray is Chief Fellow, Department of Critical Care Medicine,> > University of Pittsburgh Medical Center. Dr. Marik is Chief of Pulmonary and> > Critical Care Medicine, Thomas Jefferson University.> > Reproduction of this article is prohibited without written permission from> > the American College of Chest Physicians (e-mail: permissions at chestnet.org> > ).> > Correspondence to: Paul E. Marik, MD, FCCP, Chief of Pulmonary and> > Critical Care Medicine, Thomas Jefferson University, 1015 Chestnut Street,> > Suite M100, Philadelphia, PA 19107; e-mail: paul.marik at jefferson.eduIvanHronek MDChief, Critical Care & Trauma AnesthesiaSFMC Gas,> > Inc.Lynwood, CA 90262 Cell: 310 487-3288Pager: 310 636-6020> >> >> >> > > Date: Thu, 2 Aug 2007 11:47:10 +0200> From: markus.weis at med.lu.se> To:> > trauma-list at trauma.org> Subject: Re: Etomidate> > An editorial in> > Anaesthesia in 2005 (1) stated that etomidate had been> withdrawn in the> > United States, Australia, Canada and the Republic of> Ireland. Apparently> > this was based on information from a pharmaceutical> company and in> > correspondence (2) to the article it showed to be incorrect,> at least> > regarding it being withdrawn in the United States.> > The editorial was> > published two years ago, but sometimes rumours don't stop> circulating...> >> > BFM: What do you use instead of etomidate?> > Markus> > > (1) Morris C,> > McAllister C. Etomidate for emergency anaesthesia: mad, bad> and dangerous> > to know? Anaesthesia 2005; 60: 737-40.> (2) Jackson MT, Ramos AS. Etomidate> > - misused or misunderstood? Anaesthesia> 2006; 61: 191.> > On Thu, 02 Aug> > 2007 09:15 +0100 (BST), Blueflightmedic <> trauma at emergencyunit.com>> > wrote:> >> > Firstly congratulations to all those> > who responded so magnificently in> > Minneapolis. Condolences to the> > bereaved. The news broke here in the UK> > at 1 AM just as I was returning> > home from dealing with a very nasty> > head-on RTC; three serious, 1 died in> > my hands on scene from massive> > haemorrhage - probably ruptured liver.> >>> > > Etomidate is rapidly becoming a drug to avoid because of its prolonged> >> > suppressant effect on the adrenal response. We though initially that it> >> > was only infusions that caused the problem but there is now good evidence> >> > that a single induction dose of etomidate causes problems for some days,> >> > and patients with multiple trauma or severe sepsis do not need adrenal> >> > suppression. We scarcely ever use it now.> >> >> > > *From:* "Hardcastle,> > Tim, Dr < tch at sun.ac.za>" <tch at sun.ac.za>> > > *To:* "Trauma-List> > (E-mail)" <trauma-list at trauma.org >> > > *Date:* Thu, 2 Aug 2007 07:11:01> > +0200> > >> > > Hi all> > >> > > A query regarding Etomidate: there is a> > rumour spreading around> >> > > South Africa that Etomidate has been "black-boxed" by the FDA and> > >> > this includes a warning to not use it for RSI. I have been unable> > > to> > confirm this on their website, but maybe I don't have adequate> > > access.> > Any list member out tere form the USA who can confirm /> > > deny / give the> > correct details, so we can give clear guidelines -> > > we still use> > Etomidate for our RSI in NON-SEPTIC patients ( i.e.> > > acute trauma).> >> > >> > > My reading of the literature does not support avoiding of Etomidate>> > > > in trauma, with only one study in head trauma suggesting a possible> > >> > link.> > >> >> > BFM> > --> > 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/> >