DTIC ADA629619: Risk Factors for Hypotension in Urgently Intubated Burn Patients

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01 DEC 2012 N/A -
4. TITLE AND SUBTITLE 5a. CONTRACT NUMBER
Risk factors for hypotension in urgently intubated burn patients
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Dennis C. J., Chung K. K., Holland S. R., Yoon B. S., Milligan D. J.,
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Nitzschke S. L., Maani C. V., Hansen J. J., Aden J. K., Renz E. M.,
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United States Army Institute of Surgical Research, JBSA Fort Sam REPORT NUMBER
Houston, TX
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1184 burns 38 (2012) 1181 1185

also discovered that the maximum predicted propofol sinceahyperdynamicstateisnecessarytomaintainadequate

biophase concentration was achieved in all groups at perfusionandheartfillinginthisshockstate.Itmakessense

2.3min,regardlessofthedoseoffentanyl,propofol,orboth. thatpropofolmayhaveadramaticandenhancedhypotensive

Reich et al. sought to establish statistically significantly effectintheburnpatientsinceaknownmechanismforthis

multivariate predictors of hypotension within the 0 10min hypotension is inhibition of the SNS, upon which the burn

following induction of anesthesia [7]. It was a retrospective patientishighlydependent.Italsofollowsthathypotension

studyof2962patientsundergoinggeneralanesthesiawitha would be enhanced in burn patients during the recovery

primaryendpointofhypotensionandsecondaryendpointof periodbecausetheysufferfromincreasedvenouscapacitance

adverseeffect,mortality,andprolongedhospitalstay.Induc andsubsequenthypotensionfromdecreasedsplanchnictone,

tion agents included etomidate, propofol, thiopental, mid whichisaneffectthatpropofolexertsinallpatients,burnedor

azolam,andfentanyl.Itwasfoundthat9%ofpatientssuffered not.Finally,itseemsappropriatethatpropofolwouldhavea

severehypotensionfollowinginduction,themajorityinthe6 heightenedhypotensiveaffectinburnpatientsbecausethey

to 10 min timeframe (p<0.001). Statistically significant are,asdescribedbyBlalockin1931[10],massivelyedematous

predictorsofpost inductionhypotensionincludedASAIIIor and thus by definition hypovolemic; and multiple studies,

IV, baseline MAP <70mmHg, age (cid:3)50years, the use of including Hoka’s in 1998 [11], have associated hypovolemia

propofol,andincreasingdosesoffentanyl.Fentanylwasthe withanexaggeratedeffectonpropofol inducedhypotension.

onlyinductionagentthatshowedadose dependenteffecton Since there is a glaring paucity of data on the effects of

hypotension.Reich’sstudywasimportantbecauseitnotonly propofolinductiononburnpatients,Yamashitaetal.sought

identifiedpropofolasanindependentriskfactorforhypoten to delineate a population pharmacokinetic formula for

sionbutalsobecauseit providednewdataontheprofound propofol in burn patients that would offer a patient specific

and negative impact of even a single severe hypotensive infusion rate for sedation in the ICU during the SNS surge

episodepost induction.Thereis,infact,asignificantincrease period[12].Heinfused17burnedpatientsand19non burned

in mortality and prolonged hospital stay associated with controlswith2mg/kgpropofol(thestandardinductiondose)

clinicalhypotension,exacerbatedbythepresenceofASAIII and measured serum concentration up to 4.5min after

statusandage(cid:3)65years. administration. He found that the increased volume of

AlthoughRayetal.in2010alsofoundevidencethateven distribution typically seen in massive resuscitation and the

a single hypotensive episode post induction can lead to a enhancedrateofpropofolclearanceinburnpatientsledtoa

significant increase in morbidity and mortality, they were decreased serum propofol concentration despite dosing at

notabletocorrelatethisphenomenontopropofol[8].Their standardinductionormaintenancedoses.Alargepartofthis

studywasaretrospectiveanalysisof176patientsintubated phenomenonrelatestothefactthatthesurgeinSNSincreases

emergentlyforexploratorylaparotomiesandthenrecovered hepaticbloodflowfrom20to35mL/kg/min,thusincreasing

intheICU.ThisgroupofinvestigatorsfoundthatASAstatus propofol clearance. Percentage TBSA and body weight were

was the sole predictor for clinical hypotension. They also the two most significant covariates leading to clinical

reportedthatasASAstatusincreased,physiciansweremore hypotension. Yamashita’s work provides us data on the

likely to use etomidate or ketamine/versed (p 0.001). All appropriatedoseofpropofolformaintenanceofsedationin

induction agents utilised roughly the same amount of theICU.Unfortunately,itisdifficulttoapplythisdatatobolus

steroids and/or vasopressor support during recovery in the inductionofpropofolsincethefirst2minofthestudywere

ICU,withatrendtowardtheriskofhypotensionorneedfor notincludedinthedatatoallowforaprimarymixingphase

post intubation vasopressor usage being lower in the withincompletedistributionincentralcompartments.Little

etomidategroup. data is known about the effect of the induction of general

It is well known that burn patients experience a 10 fold anesthesia on hypotension in this context, as induction

surgeincatecholaminesduringtheirrecoveryphasepreceded happenswithin40sofapropofolbolus,andthistimeperiod

by a phase of heat induced superficial tissue damage, the wasdiscarded.

recoveryphaserepresentsischemia reperfusioninjuryrelat Based on the statistical analysis of the data, our study

ed to burn shock state and extensive intravenous fluid shows that potentially septic critically ill burned patients

resuscitation. This process amounts to a subacute hyperdy requiringintubationintheBICU,every1%increasein%TBSA

namic and hypervolemic period of convalescence during burned contributed to a 1.6% increase in the odds of the

whichthesympatheticnervoussystem(SNS)worksovertime development of hypotension. This relation was entirely

to perfuse end organs. These recovering burn patients independentofanyotherexistingfactors,includingthetype

experience a huge increase in cardiac output for weeks to ofinductionagentused,thepresenceofinhalationalinjury,

months,andtheextentofthishyperdynamicstateishighly and age. Additionally, if patients developed hypotension

associatedwith%TBSAburned,timesinceburn,thepresence following endotracheal intubation, the odds of death in

ofedema,iatrogenicdrugreactions,andseverityofinfection creasedbynearly2 fold.

and inflammation. In the early 20th century, Haldor Sneeve Thisstudyhasafewlimitationsinherenttoretrospective

proposedthatburnswouldcreateadropincardiacoutputvia studies.First,thedefinitionofhypotension(within1h)could

anaccumulationofbloodinthesplanchnicvessels[9].This beseenasproblematic,aspost inductionhypotensionusually

effectwasfromashortageofcirculatingcatecholaminesafter occursimmediatelywhenitoccurs.Thesedataweredifficult

the surge of SNS activity in the recovery period of burns. to extract accurately in a retrospective chart review of our

Sneeve advocated providing adrenaline to replete the cate electronicmedicalrecord.Thebestwecoulddowastakethe

cholaminestoresandrecoverbloodpressureinthesepatients, lowestbloodpressurerecordedduringthathourandassumeit
burns 38 (2012) 1181 1185 1185

was the one immediately post intubation. Second, the

hemodynamic response to any induction agent is typically Acknowledgments

dose dependant. We did not have consistent and accurate

documentationofvariousdosagesappliedtoanalyze.Third, TheauthorswouldliketothankOtiliaSanchezforhermedical

paralytics were used concomitantly with induction agents editingandformattingofthismanuscript.

54% of the time. This could have potentially affected our

results. Fourth, we did not evaluate volume status peri
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