Necrotic Enteritis, clostridia infection, poultry diseases, avian pathology
From Fever to Septic Shock1 (Read-Only)– DIC associated peripheral gangrene-necrotic lesions...
Transcript of From Fever to Septic Shock1 (Read-Only)– DIC associated peripheral gangrene-necrotic lesions...
4/11/16
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FromFever toSeptic Shock
https://my.vanderb i l t.edu /sep sismon ito r/p rogres s-repo rts /
Fever
http ://co l l id er.com/movie/article.asp / aid /4 8 6 7 /tcid /1
Fever• Normal human physiologic temperature rangesabove and
belowmean of ~98F(controversial)• Temperature above 99.5Fconsidered fever(also controversial)• Majorityof research todatedoes notsupport harm from
febrile state.– Threemain exceptions:• Feverd/theatstroke• Fevercausing extrememetabolic demands in ptswithunderlying cardiac and pulmonary disorders• Feverinelderlyprone tomentaldysfunction
• Research todateand variousguidelines:•Recommend onlysuppressing fevertoprovidepatientcomfort•Findan increase inviralshedding andprolonged diseasestateswithAspirinand Tylenoluse
EtiologyofFever
• Mostcommonreasonsforfeverinclude:– Infection(toagreaterextentbacterial)– Malignancies– Connectivetissue/autoimmunediseases
• Othernotascommonreasons:– Postoperative– Drugs/Medications– Undiagnosedillnesses
• Otherfactorsthatcancausefever:– Tachycardia,diurnalpatterns,ovulation,exercise,digestion,trauma,psychologicaldistress/disorders,infarction,burns,renalfailureandshock,burns,tissueinfarction,childbirth
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FeverPathophysiology
http ://d rraj ivd esaimd .com/tag/ch i l l srigo rs /
Pyrogens
• Exogenouspyrogens:– Microorganismsandtoxinsorotherproductsofmicrobialorigin,which inducemainlymacrophages toproduceendogenouspyrogens
• Endogenouspyrogens:– Cytokines (mainly IL-1,IL-6,TNF-alpha, interferonandprostaglandins)
– Antigen-antibody complexesassociatedwithcomplement
– Lymphocytederived molecules– Bileacids– Androgenic steroidmetabolites (naturalandsynthetic)
Fever inSOAP
FeverinSOAP• Exam:– PMH– Medicationreview– Recenttravel,exposuretopetsandotheranimals,otherexposure
– Familyhx:rarehereditarycausesoffever– Verifyfever:noresearchsupportforbestlocationtoverify(inadults)
– Pattern:continuous,relapsing,etc…• Labteststoconsider: CBCwithdifferential,CMP,UAC&S,CXR,ECG,ESR/CRP,ANA,Monospot,TBskintest,HIV,Heppanels
• Otherimagingperexamfindingsorindexofsuspicion
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Systemic Inflammatory ResponseSyndrome(SIRS)
• Thesystemic responsetoawide range ofstresses• Twoormoreofthe following:– Temp: >38C– HR:>90– RR:>20– PaCO2:<32– WBC:>12Kor<4K or>10%bands
SIRSDifferentialDiagnosis• Infection• Malignanthyperthermiaandheatstroke• Burns• Trauma• Pulmonaryembolism• MI• Cardiactamponade• Dissectingorrupturedaorticaneurysm• Occulthemorrhage• Adrenalinsufficiency• Thyroidstorm• Pancreatitis• Drugoverdose• Drughypersensitivityreactions
OtherSepsisDiagnostic Criteria
IDSA,2 0 1 3
• Hypothermia <36C• AMS• Significantedema or+fluidbalance• Hyperglycemia >140withDMhx• Elevated CRPand/orESR• Elevated procalcitonin• Arterial hypotension:<90SBP,MAP<70• Arterial hypoxemia:PaO2/FiO2<300• Acute oliguria:<0.5ml/kg/hr forat least2hoursdespiteadequate fluid
resuscitation• Creatinine >0.5mg/dL• Coagulationabnormalities: INR>1.5oraPTT >60• Ileus• Thrombocytopenia: plt <100K• Hyperbilirubinemia: TB>4• Decreased capillaryrefilland/ormottling• Lactic acid>2mmol/L
Elevated Lactic AcidLevels• Hyperlactatemia:>2• Lacticacidosis:>4• Twotypes– TypeA(tissuehypoxemia)
• Hypovolemia– Shock
– TypeB(withoutwidespreadtissuehypoxemia)• DKA• Sz d/o• Catecholamine release: exogenous orendogenous• Malignancy• ETOHism• Drugs:
– HAART– Propofol– Linezolid
• Mitochondrialdisorders
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Sepsis• Sepsisisthepresenceinfectiontogetherwithsystemicmanifestationsofinfection• Apartfromleukopeniaandhypothermia,sepsiscanbeanormalmanifestationofthebodiesimmuneresponseanddoesnotnecessarilysignifyaresultingpoorprognosis• Thetermsepticisaninformaltermforseveresepsisorsepticshock• Bacteremia:–Culturablebacteriainthebloodstream–Maybetransientandinconsequential–Inconsistentcorrelationwithseveresepsis
Sepsis• Leading cause ofinfectious death inU.S.• Costs ~25billion in hospital management• ~20-60% mortality rate in ~750K cases inUSannually
• >60% ofthese patients >65yearsold• ½Gram +s,½Gram (-)s, Candida• Foci ofinfection:– #1Lungs– #2“Urine”
• 100-300X greater forHD patients
SevereSepsis
IDSA,2 0 1 3
SevereSepsis•Mostcommonsitesforprimaryinfectioninpatientswithseveresepsisarethelungsandtheabdomen• Themostinfluentialfactorsforprogressingtoseveresepsis/shockare:• Surfaceareaofinfection• Severity• Susceptibilitytotreatment
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Septic Shock• Sepsiswithhypotensiondespiteadequatefluidresuscitationwithnootherunderlyingetiology
• Hypotension:<90systolic,<70MAP,or>40changefrombaseline
• Tachyphylaxistocatecholamines,corticosteroidsandaldosterone
• IncreasinglactateandH+,hyperphosphatemia• FurtherdepletionofATPstores,resultinginionpumpdysfunction:intracellulardecreaseinKandincreaseinNaandCa,leadingtocellularswelling,immenseROSactivity,cessationofproteinsynthesis,thenapoptosis
PRRs,PAMPs&DAMPs
http ://fo rmu lacro ssfi t.com/in flammato ry-r em ar ks-on -the-in flamm ato ry-p ro c es s/
PAMPs• LPS• Otherlipoproteins• Peptidoglycans• Zymosan(yeast)• Viralcoatproteins• Bacterialflagellin• Nucleicacids
*SmallsubsetofvarietyofPAMPsrepresented.WhenbindingwithPRRscreateinflammatorycascadeviareleaseofchemicalmediators(cytokines)
CellSignalingMolecules
http ://www.genecopoeia.com/p rodu ct/se ar ch /pathw ay /h_in flamP athw ay.php
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CellSignalingMolecules• Cytokines:– Eitherinflammatoryofinflammatory– Interleukins(ILs)– Interferons– Chemokines
• Histamine:– Vasodilationofmicrocirculation(capillarybeds,arterioles,venules)andvasoconstrictionoflargevessels
• Leukotrienes:– Actsimilartohistamine
• Prostaglandins:– Lipidsderivedfromcyclooxygenases(COX1,2)– Moderatecontractionofsmoothmuscles– Regulateinflammation
AcutePhaseResponse
http ://www.pharmatu to r.o rg/articles/in t erleu kin s-in -th er apeu tic s
AcutePhaseResponse• Thethreecharacteristicchangesinthemicrocirculation(arterioles,venules andcapillaries)include:–Bloodvesseldilation,increasedvascularpermeabilityandwhitebloodcellmigrationtolocalizedsiteofinnateimmunedetection(leukocytosis)
• Pain: afferentsignalsalongnociceptiveneuralpathways• Fever: IL-1,IL-6,TNF-alpha,interferonandprostaglandinsactingaspyrogens:
• Altertemperaturesetpoint,andstimulatelivertosynthesizebulkofinitialinflammatoryresponseproteins
• C-reactiveprotein:• Increasesactivityofphagocytesandfacilitatesthedeliveryofhumoral (antibodies)andcellularcomponents(TandBcells)tositesofinflammation.
AcutePhaseResponse• Anti-inflammatory:–Samemechanismscausingwhitebloodcellproliferationtoinfectedorinjuredtissuealsocanlimitabilitytoadhereandenterun-inflamedvascularendothelium.–Otherresponsesthatminimizeinflammationinclude:• Releaseofneuroendocrinehormones:cortisol,epinephrineandantioxidants
•Metabolicchanges:–IncreasedTSH,vasopressin,insulin,glucagon,catabolismofmuscleprotein
•Also:–Norepinephrine–Hepaticlipogenesis–Lipolysisinadiposetissue
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AcutePhaseResponse• Constitutional: fever, wt. loss,nightsweats, chills, rigors,myalgias, arthralgias, sleep, appetite, pain, lethargy
• HEENT: headache, photophobia,earcongestion/drainage, diplopia, conjunctivitis, rhinitis,hoarseness,pharyngitis, lymphadenopathy
• Cardio: chestpain (pleuritic),palpitations,edema
• Pulm: dyspnea,cough(+/- productive)
• GI: N/V, diarrhea, hematochezia, suppurative discharge
AcutePhaseResponse
• GU: dysuria, frequency, urgency,voidvolume,incontinence,posterior/flank pain
• MS: ROM,coordination,ataxia,muscleweakness
• Neuro: impaired mentation/consciousness, seizure,vertigo, sensation,CNimpairment
• Skin: rash/lesions,urticaria, erythrema
• Psych: depression,anxiety, mood lability
PathophysiologyofSevereSepsis• Abnormalfunctioninmicrocirculatoryunits(arterioles,venulesandcapillarybeds)
• DiminishedaccesstoO2foraerobicrespiration,thisdiminishestheATPneededforlife
• Multi-organfailureisasystem-wideorgan“hibernation”• Mismatchedratioofpro-inflammatorytoanti-inflammatorycytokines
• Desensitizationofphagocytestocomplement• Alterationofcoagulationcascades:– IncreasedtissuefactorsandVonWillibrandfactorfromincreasingcellulardebrisanddamagedendothelialtissue
– Increasedactivationofplatelets– Formationofmicrothrombi,leadingtodisseminatedintravascularcoagluation
MicrobialTriggersforSevereSepsis/Shock•Majorityofseveresepsisisassociatedwithcommensalbacterialandfungi–Entericgramnegativebacilli,coagulasenegativestaphylococci,enterococci,andCandidasp.
•Culturepositiveandculturenegativecaseshavesimilarmorbidityandmortality*•Bacterialendotoxins:–Scantevidencetheseplaylargeroleinseveresepsisbuttheystillcausesignificantcellulardamagetoareasoflocalizedextravasculartissue
• Superantigens(toxicshocksyndrometoxins):–BindtobroadrangeofTLRsviaMHCII,resultinginexcessivecytokinesandotheracutephasechemicalmediators– S.aureus,S.pyogenes,C.perfringens,V.vulnificus,filoviridae
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SevereSepsis/Septic Shock Manifestations:Nervous andEndocrine Systems
• Alterationsinhighercerebralfunctionareoftenearlymanifestationsofseveresepsis,particularlyinolderadults
• Focalneurologicalsigns:seizuresandcranialnervepalsiesarerare
• Hypothalamic-pituitaryadrenalaxis:– Bluntedreleaseofgrowthhormone,ACTH,prolactin
• Adrenalinsufficiency:– Cytokineinduceddysfunction,glucocorticoid
tachyphylaxis, prolongedinflammatorystates,hypoglycemia
• Autonomicdysfunction:– Abnormalitiesinheartrated/talterationsinsympatheticoutputortachyphylaxis
SevereSepsis/Septic Shock Manifestations:Bloodstream
• Neutrophilicleukocytosisisthenormalresponsetobacterialorfungalinfection
• Lymphocytosisinviralinfections• Thrombocytopenia• Plasmalipids:increaseintriglycerides,freefattyacidandvLDL• Glucose:initialhyperglycemiabutcanprogresstohypoglycemia• Lacticacid• Clotting:– DICin~50%ofindividualswithseveresepsis– CBCwithdiffandperipheralsmear,aPTT/PT,D-dimer,fibrinogen
SevereSepsis/Septic Shock Manifestations:Lungs
• Hyperventilationwithrespiratoryalkalosisisoneoftheearliestmanifestationsofsepsis
• ALI(acutelunginjury):PaO2/FIo2=<300• ARDS(acuterespiratorydistresssyndrome):bilat.pulm.infiltratesw/oHForPNAwithPaO2/FIo2=<200
• Diffusealveolarepithelialinjury leadingtofluidspillingintointerstitialandairspacecompartments
• Neutrophilsandmonocytesaggregatinginpulmonaryvessels• Pulmonaryshunting• Deadspacevolumeincreasesandcompliancedecreases• Intubationandmechanicalventilation
SevereSepsis/Septic ShockManifestations:GITract
• Increasedtranslocationofbacteriaintothelymphsystemandbloodstream
• Aspirationofmicrobialcontentsintothetracheobronchialtree• SmallerosionsofthegastricandduodenalmucosawhichresultsinupperGIbleeding andileus
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SevereSepsis/Septic ShockManifestations:Kidneys
• Fromminimalproteinuriatoprofoundrenalfailure• Oliguria• Azotemia• Uremia
SevereSepsis/Septic Shock Manifestations:Liver
• Cholestaticjaundice• Completehepaticfailureisrare
SevereSepsis/Septic Shock Manifestations:Skin
• Localized:pustules,cellulitis,eschar• Seedinginfections:pustules,cellulitis,petechiae• Diffuseeruptions:– Bacterialtoxins-hemorrhagiclesions– DICassociatedperipheralgangrene-necroticlesions
SevereSepsis/Septic Shock Manifestations:Immunity
• Immunedysfunction:– Highsusceptibilitytonosocomialinfectionsandcommensalinfections
– ReactivationoflatentherpessimplexandCMVoccursin~40%ofseveresepsispatients
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Surviving Sepsis
IDSA,2 0 1 3
SurvivingSepsis
• Obtainbloodculturesx2(aerobicandanaerobic)beforeadministrationofantimicrobialtherapyifdoesnotdelaytreatmentfor>45minutes• Drawculturespercutaneouslyandfromeachvascularaccessifnotplaced48hourspriortocontact• Culturesfromurine,CSF,wounds,respiratorysecretions,etc• Theadministrationofbroad-spectrumantimicrobialswithin1hourinpatientswithseveresepsisandsepticshock• Sourcecontrol:necrotizingsofttissueinfections,peritonitis,cholangitis,intestinalinfarction,intravascularaccessdevices,etcwithappropriaterapidconsultation
ContinuingSepsisTreatment• De-escalate antibiotics: targetingbothpurported species and
sensitivity• Procalcitonin• Use ofcrystalloids for fluid resuscitation, albuminwhere
substantial crystalloidsareneeded• Vasopressors:
– Norepinephrine as firstchoice (dopamine asalternativeonlyinhighlyselected patients)
– Epinephrine assecond add onorsecond choice– Vasopressin next– No lowdose dopamine forrenal protection
• Inotropic therapy:– Trialdose of dobutamine withsigns ofmyocardial dysfunction:elevatedcardiac fillingpressures, lowcardiac output
• Insome patients,hydrocortisone
Continuing Sepsis Treatment
• Tightglucosecontrol• PRBCinfusiononlywhenHgbisbelow 7g/dL• Platelets onlywhen<10Kwithoutbleeding and<20Kwithactive bleeding
• Continuousorintermittent hemodialysis• Intubationandmechanical ventilation management• Entericnutrition• Stressulcerprophylaxis• DVTprophylaxis• Decubitusulcerprophylaxis
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Sepsis Workup
• CBCwithdifferential, CMP,Mg,Phos.,IonizedCa• Lacticacid(q2until<2)• Procalcitonin• ABG• Coag.Panel, fibrinogen• CXR,UA,BCs(PCR),Resp.Cx andgram stain(PCR)• Legionella Ag, S.pneumoniae Ag• C.diff.PCR• InfluenzaA&BPCR
Procalcitonin (PCT)
• Usualcourse=cleavage intocalcitonininthyroid• Extrathyroidal non-neuroendocrinecleavage= mainlywithincreased concentrationsduringbacterial infectionbut*
• DAMPs+PAMPs= increase inlevels• Sepsisvs.SIRSofnoninfectiousorigin: LungsandGI• Levelspeak at6hours,plateau at~8-24hours,canremainelevated fordays-weeks after infection
• Differentbaselineand infectiondrivenPCT levels forCKDpatients
Procalcitonin (PCT)
Brecho t et al . , 2 0 1 5
Procalcitonin (PCT)
Grace and Tu rner,2 0 1 4
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Multiplex PCR• 1-2dayswithBCsvs hourswithPCR• AmplifiesDNAoflargespectrumofinfectiousbacteria• Decreased treatment ofcontaminants• Earlier administration ofdirectedABXsorde-escalation ofABXs
• Minimized resistance• ~25%reductionof#ofbroadspectrumdays
AntibioticResistance
http ://www.tu fts.edu /med /apua/abou t_issue /an tib io tic_r es _4 _2 8 2 6 0 3 7 9 0 3 .JPG
Anti-infective Therapy
http ://upend rats.b lo gspo t.com/2 0 1 2 /0 6 /an tib io tic-
h ttp ://www.thebody.com/con ten t/art8 7 5 .h tml
Anti-infective Therapy• Identificationoftheinfectingorganism:– Cultures,immunologicassaysandmoleculartesting(PCR)beforestartingdrugtherapy
• Inmostcases,offendingagentwillneverbefound:– Aimformostprobableoffendingagents:• Cellulitisinnon-immunocompromised individual(S.aureus,S.pyogenes)• Acuteotitismediainyoungchild(viralvs.H.influenzae,S.pneumoniae.M.catarrhalis)
• Hostfactors:– Hx ofpreviousadversereactionstoantimicrobialagents– GastricpH:absorptionincreasesordecreasesdependingon
pHanddrug– Renalfunction:• Decreasedinveryyoungchildrenandolderadults• Mostimportantrouteofeliminationforantimicrobialproducts:adjustmentneededrenalfunctionforandadequatedosing
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Anti-infective Therapy– Hepatic function:watchoutforazithromycin, Zosyn,
clindamycin,metronidazole, fluconazole,nitrofurantoin,isoniazid
– G6PD(glucose-6-phosphatedehydrogenase deficiency:hemolytic reactions tonitrofurantoin andBactrim
– DMII:hypoglycemic reactions toBactrim– Pregnancy: increased clearance, notetracyclines
(includesbreast-feeding)• Siteofinfection:drug tositeofinfection(penetrance):– Bile-concentrated, blood-brainbarrier, bone,etc– Routeofadministration:oralvs.parenteral
• Removal offoreignmaterial: prostheticsandimplants
Bacteria
http ://www.d reamstime.com/pho to s-im ag es /bac teri a.h tml
Gram+AerobicCocciGram+aerobiccocci:• Coagulasepostive (Staphyloccous aureus)• Coagulasenegative:S.epidermidis andothercommensalsStreptococcus:Lancefieldantigenandhemolyticreaction
S.pyogenes (strepthroatandnecrotizingfasciitis)S.pneumoniaeS.AgalactiaeViridans streptococci(usuallycontaminants,commensals)
Treatment:Penicillins (alltypes),Cephalosporins,Clindamycin,Vancomycin,Daptomycin,Linezolid,Orbactiv (oritavancin),Sivextro (tedizolid),Dalvance (dalbavancin)
Gram+AerobicCocci
http s://ro jo sonmed icalcl in ic.wo rdp ress.com
h ttp ://l in k.sp rin ger.com/referen cewo r ken t ry
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Gram+Aerobic Bacilli (Rods)
http ://textbooko fb acterio lo gy.n et/An th rax.h tml
• Listeriamonocytogenes
• Bacillusanthracis
Gram+AnaerobicBacilli (sporeforming)
• Clostridiumtetani• C.botulinum• C.perfringens• C.difficile
h ttp ://www.cd i ff-suppo rt.co .u k/abou t.h tm
OtherGram+
http ://o ccupational -th erap y.ad van ceweb .co m/f eatu r es/ arti cles /vr e-sti l l -re sistin g
• Enterococcusfaecalis• E.faecium
Gram(-) Aerobic Cocci
http ://www2 .wlu .edu /x5 1 8 3 4 .xml
• Neisseriameningitidis• N.gonorrhoeae• Moraxellacatarrhalis
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Gram(-) Aerobic Bacilli
http ://www.natu re.com/natu re/jou rnal/v4 0 6 /n6 7 9 5 /fig_tab/
• Vibrio cholerae• V.vulnificus• H.pylori• Pseudomonasaeruginosa
Gram(-)AerobicBacilli:Enterobacteriaceae
http ://www.mrsaidb lo g.com/tag/c arb ap enem-r esist an t-en t erobact eri ac ea e/
• E.coli• Klebsiella• Citrobacter• Enterobacter• Morganella• Proteus• Salmonella• Yersiniapestis
OtherGram(-)
http ://textbooko fb acterio lo gy.n et/h aemoph i lu s_2 .h tml
• H.Influenzae• Legionellapneumophila• Captocytophaga
canimorsus
Spirochetes
http ://news.n ationalgeograph ic.com/news/2 0 1 4 /0 2 /1 4 0 2 2 8 -
• Syphilis(Treponemapallidum)• Lymedisease(B.burgdorferi)
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Mycoses
http ://servin gnatu re.b lo gspo t.com
Viruses
http ://www.fromquarkstoquasars.com/rh inopharyngi ti s
• Lungs:– Non-Pseudomonas
• Rocephin +Azithromycin• Levaquin
– Pseudomonas• Cefepime orAztreonam +Levaquin orCarbapenem
– Pseudomonas +MRSARisk• Cefepime orAztreonam +Levaquin orCarbapenem +Vancomycin
• Meningitis– Rocephin or IDconsult +Vancomycin
• Intra-abdominal– Zosyn orLevaquin orFlagyl
Antibacterials
• Skin– Vancomycin +Clindamycin+Zosyn orAztreonam
• Line sepsis– Vancomycin +Cefepime orLevaquin
• Urine– Cefepime orAztreonam +Levaquin
• Neutropenic fevers– Vancomycin +Cefepime orAztreonam orLevaquin
Antibacterials
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• Zosyn:– Coag.abnormalities– Thrombocytopenia– Jarisch-Herxheimer reaction– Seizures(renalfailure)
• Levaquin:– QTprolongation– Cautionwithelectrolyteabnormalities– Hypoglycemia– Tendonrupture– CautioninSz d/o
Antibacterials
• Cefepime:– IncreasesINR– Encephalopathy,mycoclonus,seizures
• Rocephin– INRabnormalities
• Azithromycin– QTprolongation,cautionwithelectrolyteabnormalities– Cautionwithbradycardia,uncompensatedHF,
antiarrthymics
Antibacterials
– Azoles(voraconazole,etc)– Echinocandins (caspofungin,micafungin)– AmphotericinB– Bactrim
Antifungals• Acyclovir
• Reactivation– HSV– CMV– EBV– HepatitisB
Antivirals
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• +Fluid balanceà steadystatefluid balanceà (-)fluidbalance
• CHFandCKD
• Crystalloids– 30ml/kgbolus– maintenance fluids– NSvs LR
• Colloids– Albumin(nodefinitiveanswerfromresearch)– Starches=AKI
Fluid Resuscitation
• Greaterdendriticcellresponse=greatermagnitudeandtimeofsepsispresentation
• Glucocorticoids mutedendriticcellresponse• Duringsepsisincreasedchemicalmediator
concentrations=bluntedadrenalcorticosteroidproduction
• Additionofexogenouscorticosteroidsdecreasesmagnitudeandtruncateslengthofpresentationbutincreasesriskofrecurrentinfection
• Hydrocortisone
Corticosteroids
• Nocurrentresearchsupportedrecommendationsbutinpractice
• IndicatedforESRDorrenaltubularacidosispatientswithconcurrentsepsis
• pH<7.2• Issues– Naoverload thus fluid overloadalso– Increases lactateandpCO2 levels– Decreases ionized Ca levelswhich resultsindecreased CO
Sodium Bicarbonate• Hyperglycemic variability s/tproinflammatory
mediators (cortisol, catecholamines, cytokines)• Prothrombotic effects• Decreased endothelial vascular reactivity• Decreased function ofneutrophils
• Insulin gtt-short acting– GoalBG140-180
Dysglycemia and Sepsis
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• Netcatabolicstate– Decreased carbs, protein and lipids
• Anorexia• Encephalopathy• Mechanicalventillation
• ~6daydelayinnutritionalsupplementation– Enteral first!
Metabolism andSepsis
Englert and Rogers, 2 0 1 6
• AssociatedwithCAP– Extendeddurationoffebrilestate– Increasedlengthofhospitalstay– Increasedlikelihoodofempyemas andARDS
• Minimizesimmunefunction– Neutrophil andMacrophageactivity
• Increasedproinflammatory cytokines
• Increasedintestinalpermeability=bacterialtranslocation
• Decreasedciliaandsurfactantfunction
• Increasesriskofaspiration
• Poordentalhygiene
• Minimizescoughreflex
• Malnutrition
ETOHuse and sepsisAbouDagher,Gilbertetal. (2015).Sepsis inhemodialysis patients.BMCEmergencyMedicine, 15(30)
Brechot,Nicolas,Hekimian, Guillaume, Chastre,JeanandLuyt,Charles,Edouard.(2015).Procalcitonin toguideantibiotic therapy intheICU.InternationalJournalof Antimicrobial agents,46,S19-S24
Englert, JoshuaandRogers,Angela.(2016).Metabolism,metabolomics andnutritional supportofpatientswithsepsis. Clinics inChest Medicine
Grace, Eddie andTurner,Mackenzie. (2014).Useof procalcitonin inpatientswith various degress of chronickidney disease including renal replacement therapy.Clinical Practice,59(12) ,1761-1767
Larkin, Caroline,Santos-Martinez,Maria-Jose,Ryan,Thomas, andRadomski,Marek. (2016).Sepsis-associatedthrombocytopenia.Thrombosis Research,141,11-16
Mandell, Gerald, Bennett,JohnandDolin,Raphael,Principles andPracticeof Infectious Diseases,7thE
Plummer,MarkandDeane, Adam.(2016).Dysglycemiaandglucosecontrolduring sepsis.Clinics inChestMedicine
References
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Sasko, Benjaminetal. (2015).Earliest bedsideassessment of hemodynamic parameters andcardiac biomarkers:their roleof predictors of adverseoutcomeinpatientswith septic shock.InternationalJournalof MedicalSciences, 12(9) ,680-688
Semler, MatthewandRice,Todd.(2016).Sepsis resuscitation:f luidchoiceanddose.Clinics inChest Medicine
Robinson,Richard.(2015).Glucocorticoidsreducesepsisbydminishingdendriticcellresponses.PLOSBiology,DOI:10.1371/journal.pbio.1002270
Velisarris etal. (2015).Theuseif sodiumbicarbonateinthetreatment ofacidosis insepsis:aliteratureupdateonalongterm debate.Critical Care Research andPractice, ArticleID605830
http://survivingsepsis.org/Guidelines/Pages/default.aspx
CDC
IDSA
WHO
References