***SPAM*** Etomidate & adrenal suppress. - OK to use-may add steroids

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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/
>
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