Sepsis Syndromes in Adults

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Sepsis syndromes in adults: Epidemiology, defnitions, clinicalpresentation, diagnosis, and prognosis

AuthorRemi Neviere, MD

Literature review current through: May 2016. | This topic last updated: May 20, 2016.

INTRODUCTIONSepsis is a clinical syndrome that has physiologic, biologic, and biochemical abnormalities cased by adysreglated in!lammatory response to in!ection. Sepsis and the in!lammatory response that enses can leadto mltiple organ dys!nction syndrome and death.

EPIDEIOLO!"

Incidence

"n the late 1#$0s, it %as estimated that 16&,000 cases o! sepsis occrred in the 'nited States ('S) each year.Since then, rates o! sepsis in the 'S and else%here have dramatically increased as spported by the !ollo%ingstdies* +ne national database analysis o! discharge records !rom hospitals in the 'S estimated an annalrate o! more than 1,66,000 cases o! sepsis bet%een 1#$# and 2000. -nother retrospective poplationbasedanalysis reported increased rates o! sepsis and septic shoc/ !rom 1 to $ cases per 100,000 bet%een 1##and 200#. - retrospective analysis o! an international database reported a global incidence o! &$ per 100,000personyears !or sepsis and 2$0 per 100,000 personyears !or severe sepsis bet%een the years 1## and201, althogh this rate %as not re!lective o! contribtions !rom lo% and middleincome contries.

he increased rate o! sepsis is thoght to be a conse3ence o! advancing age, immnosppression, andmltidrgresistant in!ection. "t is also li/ely to be de to the increased detection o! early sepsis !romaggressive sepsis edcation and a%areness campaigns, althogh this hypothesis is nproven. he incidenceo! sepsis varies among the di!!erent racial and ethnic grops, bt appears to be highest among -!rican

-merican males. he incidence is also greatest dring the %inter, probably de to the increased prevalence o!respiratory in!ections. +lder patients 46 years o! age accont !or the ma5ority (60 to percent) o! allepisodes o! sepsis %ith an increasing aging poplation, it is li/ely that the incidence o! sepsis %ill contine toincrease in the !tre.

Pathogens

he contribtion o! varios in!ectios organisms to the brden o! sepsis has changed over time. 7ram positivebacteria are most !re3ently identi!ied in patients %ith sepsis in the 'nited States, althogh the nmber o!cases o! 7ram negative sepsis remains sbstantial. he incidence o! !ngal sepsis has increased over thepast decade, bt remains lo%er than bacterial sepsis.

Disease severit#he severity o! disease appears to be increasing. "n one retrospective analysis, the proportion o! patients %ithsepsis %ho also had at least one dys!nctional organ increased !rom 26 to && percent bet%een 1## and200. he most common mani!estations o! severe organ dys!nction %ere acte respiratory distresssyndrome, acte renal !ailre, and disseminated intravasclar coaglation. 8o%ever, it is nclear as to %hetherthe rising incidence o! severe sepsis and septic shoc/ re!lects the overall increased incidence o! sepsis oraltered de!initions o! sepsis over time.

PAT$OP$"%IOLO!"

he normal host response to in!ection is a comple9 process that locali:es and controls bacterial invasion, %hileinitiating the repair o! in5red tisse. "t involves the activation o! circlating and !i9ed phagocytic cells, as %ellas the generation o! proin!lammatory and antiin!lammatory mediators. Sepsis reslts %hen the response toin!ection becomes generali:ed and involves normal tisses remote !rom the site o! in5ry or in!ection.

Nor&al response to in'ectionhe host response to an in!ection is initiated %hen innate immne cells, particlarly macrophages, recogni:eand bind to microbial components. his may occr by several path%ays*

;attern recognition receptors (;RRs) on the sr!ace o! host immne cells may recogni:e and bind to

the pathogenassociated moleclar patterns (;-M;s) o! microorganisms. here are three !amilies o!
http://aplicacionesbiblioteca.udea.edu.co:2108/contents/sepsis-syndromes-in-adults-epidemiology-definitions-clinical-presentation-diagnosis-and-prognosis/contributorshttp://aplicacionesbiblioteca.udea.edu.co:2108/contents/sepsis-syndromes-in-adults-epidemiology-definitions-clinical-presentation-diagnosis-and-prognosis/contributorshttp://aplicacionesbiblioteca.udea.edu.co:2108/contents/sepsis-syndromes-in-adults-epidemiology-definitions-clinical-presentation-diagnosis-and-prognosis/contributorshttp://aplicacionesbiblioteca.udea.edu.co:2108/contents/sepsis-syndromes-in-adults-epidemiology-definitions-clinical-presentation-diagnosis-and-prognosis/contributors


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;RRs* tollli/e receptors (


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systemic in!lammatory response syndrome (S"RS). he !ocs o! or revie% is on sepsis, bt mch o! ordiscssion is applicable to S"RSSepsis can be conceptali:ed as malignant intravasclar in!lammation.

Malignant becase it is ncontrolled, nreglated, and sel!sstaining

"ntravasclar becase the blood spreads mediators that are sally con!ined to celltocell interactions

%ithin the interstitial space

"n!lammatory becase all characteristics o! the septic response are e9aggerations o! the normal

in!lammatory response"t is ncertain %hy immne responses that sally remain locali:ed sometimes spread beyond the localenvironment casing sepsis. he case is li/ely mlti!actorial and may inclde the direct e!!ects o! the invadingmicroorganisms or their to9ic prodcts, release o! large 3antities o! proin!lammatory mediators, andcomplement activation. "n addition, some individals may be genetically ssceptible to developing sepsis.

E''ects o' &icroorganis&sEacterial cell %all components (endoto9in, peptidoglycan, mramyl dipeptide, and lipoteichoic acid) and

bacterial prodcts (staphylococcal enteroto9in E, to9ic shoc/ syndrome to9in1, ;sedomonas e9oto9in -, andM protein o! hemolytic grop - streptococci) may contribte to the progression o! a local in!ection to sepsis.his is spported by the !ollo%ing observations regarding endoto9in, a lipopolysaccharide !ond in the cell %allo! gram negative bacteria*

=ndoto9in is detectable in the blood o! septic patients.

=levated plasma levels o! endoto9in are associated %ith shoc/ and mltiple organ dys!nction

=ndoto9in reprodces many o! the !eatres o! sepsis %hen it is in!sed into hmans, incldingactivation o! the complement, coaglation, and !ibrinolytic systems. hese e!!ects may lead tomicrovasclar thrombosis and the prodction o! vasoactive prodcts, sch as brady/inin.

E(cess proin'la&&ator# &ediators


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%#ste&ic E''ects O' %epsisFidespread celllar in5ry may occr %hen the immne response becomes generali:ed celllar in5ry is theprecrsor to organ dys!nction. he precise mechanism o! celllar in5ry is not nderstood, bt its occrrenceis indisptable as atopsy stdies have sho%n %idespread endothelial and parenchymal cell in5ry.Mechanisms proposed to e9plain the celllar in5ry inclde* tisse ischemia (ins!!icient o9ygen relative too9ygen need), cytopathic in5ry (direct cell in5ry by proin!lammatory mediators and>or other prodcts o!

in!lammation), and an altered rate o! apoptosis (programmed cell death).

Tissue ische&iaSigni!icant derangement in metabolic atoreglation, the process that matches o9ygen availability to changingtisse o9ygen needs, is typical o! sepsis. "n addition, microcirclatory and endothelial lesions !re3entlydevelop dring sepsis. hese lesions redce the crosssectional area available !or tisse o9ygen e9change,disrpting tisse o9ygenation and casing tisse ischemia and celllar in5ry*

GMicrocirclatory lesions he microcirclatory lesions may be the reslt o! imbalances in the

coaglation and !ibrinolytic systems, both o! %hich are activated dring sepsis.

G=ndothelial lesions he endothelial lesions may be a conse3ence o! interactions bet%een

endothelial cells and activated polymorphonclear le/ocytes (;MNs). he increase in receptormediated netrophilendothelial cell adherence indces the secretion o! reactive o9ygen species, lyticen:ymes, and vasoactive sbstances (nitric o9ide, endothelin, plateletderived gro%th !actor, andplatelet activating !actor) into the e9tracelllar milie, %hich may in5re the endothelial cells. or other prodcts o! in!lammation may case sepsis indced mitochondrialdys!nction (eg, impaired mitochondrial electron transport) via a variety o! mechanisms, inclding directinhibition o! respiratory en:yme comple9es, o9idative stress damage, and mitochondrial DN- brea/do%n. Schmitochondrial in5ry leads to cytoto9icity. here are several lines o! evidence that spport this belie!*

?ell cltre e9periments have sho%n that endoto9in, N@a, and nitric o9ide case

destrction and>or dys!nction o! inner membrane and matri9 mitochondrial proteins, !ollo%ed bydegeneration o! the mitochondrial ltrastrctre. hese changes are !ollo%ed by measrable changesin other celllar organelles by several hors. he end reslt is !nctional impairment o! mitochondrialelectron transport, disordered energy metabolism, and cytoto9icity.

Stdies sing varios animal models have !ond normal or spranormal o9ygen tension in organs

dring sepsis, sggesting impaired o9ygen tili:ation at the mitochondrial level. -s e9amples, a stdyin resscitated endoto9emic pigs !ond a spranormal ileomcosal o9ygen tension, %hile a stdy inendoto9emic rats !ond an elevated o9ygen tension in the bladder epithelim.

he clinical relevance o! mitochondrial dys!nction in septic shoc/ %as sggested by a stdy o! 2 critically illseptic patients %ho nder%ent s/eletal mscle biopsy %ithin 2& hors o! admission to the "?'. S/eletal mscle

-; concentrations, a mar/er o! mitochondrial o9idative phosphorylation, %ere signi!icantly lo%er in the 12patients %ho died o! sepsis than in 16 srvivors. "n addition, there %as an association bet%een nitric o9ideoverprodction, antio9idant depletion, and severity o! clinical otcome. hs, cell in5ry and death in sepsismay be e9plained by cytopathic (or histoto9ic) ano9ia, %hich is an inability to tili:e o9ygen even %hen present.Mitochondria can be repaired or regenerated by a process called biogenesis. Mitochondrial biogenesis mayprove to be an important therapetic target, potentially accelerating organ dys!nction and recovery !romsepsis.

Apoptosis-poptosis (also called programmed cell death) describes a set o! reglated physiologic and morphologiccelllar changes leading to cell death. his is the principal mechanism by %hich senescent or dys!nctionalcells are normally eliminated and the dominant process by %hich in!lammation is terminated once an in!ectionhas sbsided. Dring sepsis, proin!lammatory cyto/ines may delay apoptosis in activated macrophages andnetrophils, thereby prolonging or agmenting the in!lammatory response and contribting to the developmento! mltiple organ !ailre. Sepsis also indces e9tensive lymphocyte and dendritic cell apoptosis, %hich altersthe immne response e!!icacy and reslts in decreased clearance o! invading microorganisms. -poptosis o!lymphocytes has been observed at atopsies in both animal and hman sepsis. he e9tent o! lymphocyteapoptosis correlates %ith and the severity o! the septic syndrome and the level o! immnosppression.


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-poptosis has been also observed in parenchymal cells, endothelial, and epithelial cells. Several e9perimentsstdies sho% that inhibiting apoptosis protect animal !rom organ dys!nction and lethality.itochondrial d#s'unction in sepsis+induced &ultiple organ 'ailure"n patients dying !rom sepsis, light and electron microscopy as %ell as immnohistochemical staining !ormar/ers o! celllar in5ry and stress, revealed that cell death %as rare in sepsisindced heart and renaldys!nction. Moreover, the degree o! cell in5ry death did not accont !or severity o! sepsisindced organdys!nction. he presence o! sbtle mitochondrial morphological changes cold indicate that mitochondrial

energetic crisis (metabolic sbstrate tili:ation and mitochondrial +9;hos machinery pertrbations) may beinvolved in organ dys!nction, in the absence o! cell death.

I&&unosuppression?linical observations and animal stdies sggest that the e9cess in!lammation o! sepsis may be !ollo%ed byimmnosppression. -mong the evidence spporting this hypothesis, an observational stdy removed thespleens and lngs !rom &0 patients %ho died %ith active severe sepsis and then compared them %ith thespleens !rom 2# control patients and the lngs !rom 0 control patients. he median dration o! sepsis %as!or days. he secretion o! proin!lammatory cyto/ines (ie, tmor necrosis !actor, inter!eron gamma, interle/in6, and interle/in10) !rom the splenocytes o! patients %ith severe sepsis %as generally less than 10 percentthat o! controls, !ollo%ing stimlation %ith either anti?D>anti?D2 or lipopolysaccharide. Moreover, the cells!rom the lngs and spleens o! patients %ith severe sepsis e9hibited increased e9pression o! inhibitoryreceptors and ligands, as %ell as e9pansion o! sppressor cell poplations, compared %ith cells !rom controlpatients. he inability to secrete proin!lammatory cyto/ines combined %ith enhanced e9pression o! inhibitoryreceptors and ligands sggests clinically relevant immnosppression.

Organ+%peci'ic E''ects O' %epsishe celllar in5ry described above, accompanied by the release o! proin!lammatory and antiin!lammatorymediators, o!ten progresses to organ dys!nction. No organ system is protected !rom the conse3ences o!sepsis those listed inclded in this section are the organ systems that are most o!ten involved. Mltiple organdys!nction is common.

Circulation8ypotension de to di!!se vasodilation is the most severe e9pression o! circlatory dys!nction in sepsis. "t isprobably an nintended conse3ence o! the release o! vasoactive mediators, %hose prpose is to improvemetabolic atoreglation (the process that matches o9ygen availability to changing tisse o9ygen needs) byindcing appropriate vasodilation. Mediators inclde the vasodilators prostacyclin and nitric o9ide (N+), %hichare prodced by endothelial cells. N+ is believed to play a central role in the vasodilation accompanying septicshoc/, since N+ synthase can be indced by incbating vasclar endothelim and smooth mscle %ithendoto9in. Fhen N+ reaches the systemic circlation, it depresses metabolic atoreglation at all o! the

central, regional, and microregional levels o! the circlation. "n addition, N+ may trigger an in5ry in the centralnervos system that is locali:ed to areas that reglate atonomic control. -nother !actor that may contribte tothe persistence o! vasodilation dring sepsis is impaired compensatory secretion o! antidiretic hormone(vasopressin). his hypothesis is spported by a stdy that !ond that plasma vasopressin levels %ere lo%er inpatients %ith septic shoc/ than in patients %ith cardiogenic shoc/ (.1 verss 22.$ pg>m


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capillary density. his may be de to e9trinsic compression o! the capillaries by tisse edema,endothelial s%elling,and>or plgging o! the capillary lmen by le/ocytes or red blood cells (%hich losetheir normal de!ormability properties in sepsis).

-t the level o! the endothelim, sepsis indces phenotypic changes to endothelial cells. his occrs

throgh direct and indirect interactions bet%een the endothelial cells and components o! the bacterial%all. hese phenotypic changes may case endothelial dys!nction, %hich is associated %ithcoaglation abnormalities redced le/ocytes, decreased red blood cell de!ormability, preglation o!

adhesion molecles, adherence o! platelets and le/ocytes, and degradation o! the glycocaly9strctre. Di!!se endothelial activation leads to %idespread tisse edema, %hich is rich in protein.Microparticles !rom circlating and vasclar cells also participate in the deleterios e!!ects o! sepsisindcedintravasclar in!lammation.

Lung=ndothelial in5ry in the plmonary vasclatre dring sepsis distrbs capillary blood !lo% and enhancesmicrovasclar permeability, reslting in interstitial and alveolar plmonary edema. Netrophil entrapment %ithinthe lngIs microcirclation initiates and>or ampli!ies the in5ry in the alveolocapillary membrane. he reslt isplmonary edema, %hich creates ventilationper!sion mismatch and leads to hypo9emia. Sch lng in5ry isprominent dring sepsis, li/ely re!lecting the lngIs large microvasclar sr!ace area. -cte respiratory distresssyndrome is a mani!estation o! these e!!ects.

!astrointestinal tracthe circlatory abnormalities typical o! sepsis may depress the gtIs normal barrier !nction, allo%ing

translocation o! bacteria and endoto9in into the systemic circlation (possibly via lymphatics, rather than theportal vein) and e9tending the septic response. his is spported by animal models o! sepsis, as %ell as aprospective cohort stdy that !ond that increased intestinal permeability (determined !rom the rinarye9cretion o! orally administered lactloseand mannose) %as predictive o! the development o! mltiple organdys!nction syndrome.

Liverhe reticloendothelial system o! the liver normally acts as the !irst line o! de!ense in clearing bacteria andbacteriaderived prodcts that have entered the portal system !rom the gt. or hypo9emiais one mechanism. 8o%ever, systemic hypotension, direct renal vasoconstriction, release o! cyto/ines (eg,tmor necrosis !actor), and activation o! netrophils by endoto9in and @M


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!nctional ?NS changes, as measred throgh somatosensory evo/ed potentials. "n addition to thesenerological conse3ences o! sepsis, there is gro%ing recognition that the parasympathetic nervos systemmay be a mediator o! systemic in!lammation dring sepsis. his is spported by nmeros observations invarios animal models. -!!erent vags nerve stimlation dring sepsis increases the secretion o! corticotropinreleasing hormone (?R8), -?8, and cortisol the last e!!ect can be sppressed by sbdiaphragmaticvagotomy. ;arasympathetic tone a!!ects thermoreglation, as e9perimental vagotomy attenates thehyperthermic response to "=S"?M tas/ !orce as anincrease o! t%o or more points in theS+@- score.he validity o! this score %as derived !rom criticallyillpatients %ith sspected sepsis by interrogating over a million intensive care nit ("?') electronic healthrecord enconters !rom "?'s both inside and otside the 'nited States A22$B. "?' patients %eresspected as having in!ection i! body !lids %ere cltred and they received antibiotics. ;redictive scores(S+@-, systemic in!lammatory response syndrome AS"RSB, and logistic +rgan Dys!nction SystemA


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strategies nor does it predict mortality based pon demographics (eg, age) or nderlying condition (eg,stem cell transplant recipient verss postoperative patient). S+@- and other predictive scores arediscssed separately. (SeeL;redictive scoring systems in the intensive care nitL, section on ISe3ential(sepsisrelated) +rgan @ailre -ssessment (S+@-)I.)GIn'ection here are no clear gidelines to help the clinician identi!y the presence o! in!ection or tocasally lin/ an identi!ied organism %ith sepsis. "n or e9perience, !or this component o! the diagnosis,the clinician is reliant pon clinical sspicion derived !rom the signs and symptoms o! in!ection as %ell as

spporting radiologic and microbiologic data and response to therapy.

he term severe sepsis, %hich originally re!erred to sepsis that %as associated %ith tisse hypoper!sion (eg,elevated lactate, oligria) or organ dys!nction (eg, elevated creatinine, coaglopathy) A 1&,2B, is no longersed since the 2016 sepsis and septic shoc/ de!initions inclde patients %ith evidence o! tisse hypoper!sionand organ dys!nction.

%eptic shoc.J Septic shoc/ is a type o! vasodilatory or distribtive shoc/. Septic shoc/is de!ined as sepsisthat has circlatory, celllar, and metabolic abnormalities that are associated %ith a greater ris/ o! mortalitythan sepsis alone A2B. ?linically, this incldes patients %ho !l!ill the criteria !or sepsis (seeISepsisIabove)%ho, despite ade3ate !lid resscitation, re3ire vasopressors to maintain a mean arterial pressre (M-;)46 mm8g and have a lactate 2 mmol>< (1 mg>d


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GAdvanced age 0123 #ears4 he incidence o! sepsis is disproportionately increased in older adltpatients and age is an independent predictor o! mortality de to sepsis. Moreover, older adlt nonsrvivors tend to die earlier dring hospitali:ation and older adlt srvivors more !re3ently re3ires/illed nrsing or rehabilitation a!ter hospitali:ation A&0B.GI&&unosuppression ?omorbidities that depress hostde!ense (eg, neoplasms, renal !ailre, hepatic!ailre, -"DS, asplenism) and immnosppressant medications are common among patients %ith sepsis,severe sepsis, or septic shoc/.

GDia)etes and cancer Diabetes and some cancers may alter the immne system, reslt in anelevated ris/ !or developing sepsis, and increase the ris/ o! nosocomial sepsis.GCo&&unit# ac5uired pneu&onia Severe sepsis and septic shoc/ develop in appro9imately & and percent, respectively, o! patients hospitali:ed %ith commnityac3ired pnemonia A&1B.GPrevious hospitali6ation 8ospitali:ation is thoght to indce an altered hman microbiome,particlarly in patients %ho are treated %ith antibiotics. ;revios hospitali:ation has been associated %itha three!old increased ris/ o! developing severe sepsis in the sbse3ent #0 days A&2B. ;atients %ithhospitali:ations !or in!ectionrelated conditions, especially Clostridium difficile in!ection, are at greatestris/.G!enetic 'actors Eoth e9perimental and clinical stdies have con!irmed that genetic !actors canincrease the ris/ o! in!ection. "n !e% cases, monogenic de!ects nderlie vlnerability to speci!ic in!ection,bt genetic !actors are typically genetic polymorphisms. 7enetic stdies o! ssceptibility to in!ection haveinitially !ocsed on de!ects o! antibody prodction, or a lac/ o! cells, phagocytes, natral /iller cells, orcomplement. Recently, genetic de!ects have been identi!ied that impair recognition o! pathogens by theinnate immne system, increasing ssceptibility to speci!ic classes o! microorganisms A&B.

CLINICAL PRE%ENTATION

;atients %ith sspected or docmented sepsis typically present %ith hypotension, tachycardia, !ever, andle/ocytosis. -s severity %orsens, signs o! shoc/ (eg, cool s/in and cyanosis) and organ dys!nction develop(eg, oligria, acte /idney in5ry, altered mental stats) A1&,2B. "mportantly, the presentation is nonspeci!icsch that many other conditions (eg, pancreatitis, acte respiratory distress syndrome) may present similarly.Detailed discssion o! the clinical !eatres o! shoc/ are discssed separately.

%#&pto&s and signsJ he symptoms and signs o! sepsis are nonspeci!ic bt may inclde the !ollo%ing*GSymptoms and signs speci!ic to an in!ectios sorce (eg, cogh dyspnea may sggest pnemonia,pain and prlent e9date in a srgical %ond may sggest an nderlying abscess)G-rterial hypotension (eg, systolic blood pressre ASE;B #0 mm8g, mean arterial pressre AM-;B $0mm8g, an SE; decrease &0 mm8g, or less than t%o standard deviations belo% normal !or age)Gemperatre . or 6O?

G8eart rate #0 beats>min or more than t%o standard deviations above the normal vale !or ageGachypnea, respiratory rate 20 breaths>minG-ltered mental statsG"les (absent bo%el sonds o!ten an endstage sign o! hypoper!sion)GDecreased capillary re!ill, cyanosis, or mottling (may indicate shoc/)

La)orator# signsJ Similarly, laboratory !eatres are nonspeci!ic and may be associated %ith abnormalitiesde to the nderlying case o! sepsis or to tisse hypoper!sion or organ dys!nction !rom sepsis. heyinclde the !ollo%ing*

Ghor !or at least t%o hors despite ade3ate !lid resscitation)G?reatinine increase 0. mg>d< or &&.2 micromol>mm%as !ond to be an early prognostic mar/er o! 2daymortality in another stdy o! 1&6 patients %ith septic shoc/ A $B. "n another retrospective analysis o! criticallyill septic patients, hyperchloremia (?l 4110 m=3>or immne sppression A0,B. -ge is probably a ris/ !actor !ormortality becase o! its association %ith comorbid illnesses, impaired immnologic responses, malntrition,increased e9posre to potentially resistant pathogens in nrsing homes, and increased tili:ation o! medicaldevices, sch as ind%elling catheters and central venos lines A1,12,&B. "nability to clot has also beenassociated %ith increased mortality. "n one prospective stdy o! 260 patients %ith severe sepsis, indicators o!hypocoaglability sing standard and !nctional levels o! !ibrinogen, %ere associated %ith a si9!old increase inthe ris/ o! death, particlarly in patients treated %ith hydro9yethyl starch A$6B.

%ite o' in'ectionJ he site o! in!ection in patients %ith sepsis may be an important determinant o! otcome,%ith sepsis !rom a rinary tract in!ection generally being associated %ith the lo%est mortality rates A $,B. +nestdy !ond that mortality !rom sepsis %as 0 to percent %hen the sorce o! in!ection %as n/no%n,gastrointestinal, or plmonary, compared %ith only 0 percent %hen the sorce o! in!ection %as the rinarytract AB. -nother retrospective, mlticenter cohort stdy o! nearly 000 patients %ith septic shoc/ reportedsimilar reslts %ith the highest mortality in those %ith sepsis !rom ischemic bo%el ($ percent) and the lo%est

rates in those %ith obstrctive ropathyassociated rinary tract in!ection (26 percent) A&B. -ppro9imately 0percent o! patients %ith severe sepsis are bacteremic at the time o! diagnosis according to one stdy A6B. hisis consistent %ith a stdy o! ,$0 hospital admissions, %hich !ond that the incidence o! positive bloodcltres increased along a continm, ranging !rom 1$ percent o! patients %ith sepsis to 6# percent %ith septicshoc/ A$B. 8o%ever, the presence or absence o! a positive blood cltre does not appear to in!lence theotcome, sggesting that prognosis is more closely related to the severity o! sepsis than the severity o! thenderlying in!ection A$,B.

T#pe o' in'ectionJ Sepsis de to nosocomial pathogens has a higher mortality than sepsis de tocommnityac3ired pathogens A#,#0B. "ncreased mortality is associated %ith bloodstream in!ections de tomethicillinresistant staphylococcs ares (odds ratio 2.$0, #Q ?" 2.0.), noncandidal !ngs (oddsratio 2.66, #Q ?" 1.2$.), candida (odds ratio 2.2 #Q ?" 1.21&.&), methicillinsensitive staphylococcsares (odds ratio 1.#, #Q ?" 1.2.6), and psedomonas (odds ratio 1.6, #Q ?" 1.0&2.&$), as %ell aspolymicrobial in!ections (odds ratio 1.6#, #Q ?" 1.2&2.0) A#,#1B. Fhen bloodstream in!ections becomesevere (ie, severe sepsis or septic shoc/), the otcome is similar regardless o! %hether the pathogens are7ramnegative or 7rampositive bacteria A,#2B.

Anti&icro)ial therap#J Stdies have sho%n that the early administration o! appropriate antibiotic therapy(ie, antibiotics to %hich the pathogen is sensitive) has a bene!icial impact on bacteremic sepsis A$,B. "n onereport, early instittion o! ade3ate antibiotic therapy %as associated %ith a 0 percent redction in themortality rate compared to antibiotic therapy to %hich the in!ecting organisms %ere resistant A$B. "n contrast,prior antibiotic therapy (ie, antibiotics %ithin the past #0 days) may be associated %ith increased mortality, atleast among patients %ith 7ram negative sepsis A#B. his is probably becase patients %ho have receivedprior antibiotic therapy are more li/ely to have higher rates o! antibiotic resistance, ma/ing it less li/ely that
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appropriate antibiotic therapy %ill be chosen empirically. =mpiric antibiotic regimens !or patients %ith sspectedsepsis are discssed separately.Restoration o' per'usionJ @ailre to aggressively try to restore per!sion early (ie, !ailre to initiate earlygoaldirected therapy) may also be associated %ith mortality A#&B. - severely elevated lactate (& mmol>


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T%E'A#EUTI$ #'IO'ITIESThe earlyadministration o fuids and antibiotics is the cornerstone o management or patients#ith severe sepsis and septic shock.Therapeutic priorities or patients #ith severe sepsis or septic shock include*

$arly initiation o supportive care to correct physiologic abnormalities, such ashypo%emia and hypotension

(istinguishing sepsis rom systemic infammatory response syndrome +S'S- +table 1-because, i an inection e%ists, it must be identi)ed and treated as soon as possible +table-. This may re/uire appropriate antibiotics as #ell as a surgical procedure +eg,drainage-.

EA'L( ANA!EENTThe )rst priority in any patient #ith severe sepsis or septic shock is stabilization o their air#ayand breathing. 0e%t, perusion to the peripheral tissues should be restored and antibioticsadministered.

Sta)ili*e respiration Supplemental o%ygen should be supplied to all patients #ith sepsis ando%ygenation should be monitored continuously #ith pulse o%imetry. 'ntubation and mechanicalventilation may be re/uired to support the increased #ork o breathing that typicallyaccompanies sepsis, or or air#ay protection since encephalopathy and a depressed level oconsciousness re/uently complicate sepsis 211,13.The choice and use o sedative and induction agents +eg, etomidate,ketamine- used to intubatepatients #ith severe sepsis or septic shock are discussed separately. Other aspects o intubationand mechanical ventilation are similarly described else#here. 4hest radiographs and arterialblood gas analysis should be obtained ollo#ing initial stabilization. These studies are used incombination #ith other clinical parameters to diagnose acute respiratory distress syndrome+5(S-, #hich re/uently complicates sepsis.
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Assess per+usion Once the patients respiratory status has been stabilized, the ade/uacy operusion should be assessed. 7ypotension is the most common sign but critical hypoperusioncan also occur in the absence o hypotension, especially during early sepsis. 4linical signs oimpaired perusion include the ollo#ing*

%ypotension8 7ypotension is the most common indicator that perusion is inade/uate+eg, systolic blood pressure 2S9:3 ;

decrease in S9: >&! mm7g-. Thereore, it is important that the blood pressure beassessed early and oten. 9ecause a sphygmomanometer may be unreliable inhypotensive patients, an arterial catheter may be inserted i blood pressure is labile orrestoration o arterial perusion pressures is e%pected to be a protracted process 2?3.5ttempts to insert an arterial line should not delay the prompt management o shock.

Signs o+ poor endorgan per+usion8 @arm, fushed skin may be present in the earlyphases o sepsis. 5s sepsis progresses to shock, the skin may become cool due toredirection o blood fo# to core organs. 5dditional signs o hypoperusion includetachycardia >

guide therapy. 5dditional studies and clinical e%perience are needed.

Esta)lis. -enous access Fenous access should be established as soon as possible inpatients #ith suspected sepsis. @hile peripheral venous access may be suHcient in somepatients, particularly or initial resuscitation, the maIority #ill re/uire central venous access atsome point during their course. 5 central venous catheter +4F4- can be used to inuseintravenous fuids, medications +particularly vasopressors-, and blood products, as #ell as todra# blood or re/uent laboratory studies. 'n addition, this access can be used or hemodynamicmonitoring by measuring the central venous pressure +4F:- and the central venouso%yhemoglobin saturation +ScvO-. @hile in the past, a maIor purpose o a 4F4 #as themeasurement o ScFOand 4F:, evidence rom randomized trials on the value these targets toollo# therapeutic eJect is conficting 21


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Intra-enous /uids 'n patients #ith sepsis, intravascular hypovolemia is typical and may besevere, re/uiring rapid fuid resuscitation.

Volume The optimal volume o resuscitative fuid is unkno#n. Several studies o early goaldirected therapy reported intravenous fuid inusions targeted to physiologic endpoints andresulted in volumes ranging rom D to liters 21
http://aplicacionesbiblioteca.udea.edu.co:2108/contents/evaluation-and-management-of-suspected-sepsis-and-septic-shock-in-adults/abstract/19-21http://aplicacionesbiblioteca.udea.edu.co:2108/contents/evaluation-and-management-of-suspected-sepsis-and-septic-shock-in-adults/abstract/19http://aplicacionesbiblioteca.udea.edu.co:2108/contents/evaluation-and-management-of-suspected-sepsis-and-septic-shock-in-adults/abstract/20,21http://aplicacionesbiblioteca.udea.edu.co:2108/contents/evaluation-and-management-of-suspected-sepsis-and-septic-shock-in-adults/abstract/9http://aplicacionesbiblioteca.udea.edu.co:2108/contents/furosemide-drug-information?source=see_linkhttp://aplicacionesbiblioteca.udea.edu.co:2108/contents/evaluation-and-management-of-suspected-sepsis-and-septic-shock-in-adults/abstract/27http://aplicacionesbiblioteca.udea.edu.co:2108/contents/evaluation-and-management-of-suspected-sepsis-and-septic-shock-in-adults/abstract/28-30http://aplicacionesbiblioteca.udea.edu.co:2108/contents/pentastarch-drug-information?source=see_linkhttp://aplicacionesbiblioteca.udea.edu.co:2108/contents/evaluation-and-management-of-suspected-sepsis-and-septic-shock-in-adults/abstract/31-38http://aplicacionesbiblioteca.udea.edu.co:2108/contents/albumin-solution-drug-information?source=see_linkhttp://aplicacionesbiblioteca.udea.edu.co:2108/contents/albumin-solution-drug-information?source=see_linkhttp://aplicacionesbiblioteca.udea.edu.co:2108/contents/evaluation-and-management-of-suspected-sepsis-and-septic-shock-in-adults/abstract/31http://aplicacionesbiblioteca.udea.edu.co:2108/contents/evaluation-and-management-of-suspected-sepsis-and-septic-shock-in-adults/abstract/32http://aplicacionesbiblioteca.udea.edu.co:2108/contents/evaluation-and-management-of-suspected-sepsis-and-septic-shock-in-adults/abstract/33http://aplicacionesbiblioteca.udea.edu.co:2108/contents/pentastarch-drug-information?source=see_linkhttp://aplicacionesbiblioteca.udea.edu.co:2108/contents/evaluation-and-management-of-suspected-sepsis-and-septic-shock-in-adults/abstract/34http://aplicacionesbiblioteca.udea.edu.co:2108/contents/albumin-solution-drug-information?source=see_linkhttp://aplicacionesbiblioteca.udea.edu.co:2108/contents/albumin-solution-drug-information?source=see_linkhttp://aplicacionesbiblioteca.udea.edu.co:2108/contents/albumin-solution-drug-information?source=see_linkhttp://aplicacionesbiblioteca.udea.edu.co:2108/contents/pentastarch-drug-information?source=see_linkhttp://www.sccm.org/Documents/SSC-Guidelines.pdfhttp://www.sccm.org/Documents/SSC-Guidelines.pdfhttp://aplicacionesbiblioteca.udea.edu.co:2108/contents/evaluation-and-management-of-suspected-sepsis-and-septic-shock-in-adults/abstract/19-21http://aplicacionesbiblioteca.udea.edu.co:2108/contents/evaluation-and-management-of-suspected-sepsis-and-septic-shock-in-adults/abstract/19http://aplicacionesbiblioteca.udea.edu.co:2108/contents/evaluation-and-management-of-suspected-sepsis-and-septic-shock-in-adults/abstract/20,21http://aplicacionesbiblioteca.udea.edu.co:2108/contents/evaluation-and-management-of-suspected-sepsis-and-septic-shock-in-adults/abstract/9http://aplicacionesbiblioteca.udea.edu.co:2108/contents/furosemide-drug-information?source=see_linkhttp://aplicacionesbiblioteca.udea.edu.co:2108/contents/evaluation-and-management-of-suspected-sepsis-and-septic-shock-in-adults/abstract/27http://aplicacionesbiblioteca.udea.edu.co:2108/contents/evaluation-and-management-of-suspected-sepsis-and-septic-shock-in-adults/abstract/28-30http://aplicacionesbiblioteca.udea.edu.co:2108/contents/pentastarch-drug-information?source=see_linkhttp://aplicacionesbiblioteca.udea.edu.co:2108/contents/evaluation-and-management-of-suspected-sepsis-and-septic-shock-in-adults/abstract/31-38http://aplicacionesbiblioteca.udea.edu.co:2108/contents/albumin-solution-drug-information?source=see_linkhttp://aplicacionesbiblioteca.udea.edu.co:2108/contents/albumin-solution-drug-information?source=see_linkhttp://aplicacionesbiblioteca.udea.edu.co:2108/contents/evaluation-and-management-of-suspected-sepsis-and-septic-shock-in-adults/abstract/31http://aplicacionesbiblioteca.udea.edu.co:2108/contents/evaluation-and-management-of-suspected-sepsis-and-septic-shock-in-adults/abstract/32http://aplicacionesbiblioteca.udea.edu.co:2108/contents/evaluation-and-management-of-suspected-sepsis-and-septic-shock-in-adults/abstract/33http://aplicacionesbiblioteca.udea.edu.co:2108/contents/pentastarch-drug-information?source=see_linkhttp://aplicacionesbiblioteca.udea.edu.co:2108/contents/evaluation-and-management-of-suspected-sepsis-and-septic-shock-in-adults/abstract/34http://aplicacionesbiblioteca.udea.edu.co:2108/contents/albumin-solution-drug-information?source=see_linkhttp://aplicacionesbiblioteca.udea.edu.co:2108/contents/albumin-solution-drug-information?source=see_linkhttp://aplicacionesbiblioteca.udea.edu.co:2108/contents/pentastarch-drug-information?source=see_linkhttp://www.sccm.org/Documents/SSC-Guidelines.pdf


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Vasopressors Fasopressors are second line agents in the treatment o severe sepsis andseptic shockM #e preer intravenous fuids as long as they increase perusion #ithout seriouslyimpairing gas e%change 2D


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Static or dynamic predictors o fuid responsiveness, eg, 4F: ? to 1 mm7g #hen centralaccess is available +static measurement- or respiratory changes in the radial artery pulsepressure +dynamic measurement-.

4entral venous +superior vena cava- o%yhemoglobin saturation +ScvO- E=! percent+#hen central access is available- or mi%ed venous o%yhemoglobin saturation +SvO - E6percent +i a pulmonary artery catheter is being used-.

Cactate clearance should be ollo#ed as a target in patients #ith sepsis to ensure a trend that

demonstrates ade/uate clearance #ith therapy. 0e#er point o care analyzers are commerciallyavailable that may allo# clinicians to ollo# lactate levels at the bedside more readily 2&=A&


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pulse #aveorm analysis, or pulmonary artery catheterization- is a sensitive and speci)cpredictor o fuid responsiveness 2613. Carge randomized studies #ill be needed provingthe eHcacy o assessing dynamic measurement in response to intravenous fuids beorethey can be routinely applied to patients or the management o sepsis.

#rotocoldirected t.erapy :rotocols targeted at the use o a combination o physiologicendpoints to guide fuid management in patients #ith severe sepsis and septic shock are

common practice 21

One e%planation or the apparent negative results rom these three trials may be that central lineplacement #as common +>! percent- in patients receiving protocolAbased standard therapy andusual careM it is likely that 4F: and ScvO#ere measured and targeted in these patients as #ell.Cack o bene)t may also be attributed to overall better outcomes in these studies, perhaps dueto early administration o antibiotics +=! to 1!! percent beore randomization- in all groups, andto improved clinical perormance by highly trained clinicians in academic centers during an erathat ollo#s an aggressive sepsis education and management campaign.

Timing and duration The early administration o fuid appears to be more important thanvolume or type o fuid in reducing mortality associated #ith sepsis. 9ased upon evidence romrandomized studies and metaAanalyses, #e avor the initiation o fuid resuscitation#ithin si0hours o presentation. Once the targets o resuscitation are met and perusion isrestored, fuids can be reduced or stopped, and occasionally patients can be diuresed, #hennecessary. esolution o severe sepsis and septic shock can take as little as a e# hours or can beprotracted to days or #eeks.

5 !!? metaAanalysis o randomized trials that initiated resuscitation targeting speci)cphysiologic endpoints reported that compared to standard care, only trials that initiatedresuscitation #ithin & hours o the onset o sepsis sho#ed a mortality bene)t +D< versus =percent, odds ratio !.!,


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ade/uacy o the above therapies, antimicrobial regimen, and control o the septic ocus,as #ell as the accuracy o the diagnosis and the possibility that une%pectedcomplications or coe%isting problems have intervened +eg, pneumothora% ollo#ing 4F4insertion-.

UAde2uate per+usion8 :atients #ho respond to therapy should have the rate o fuidadministration reduced or stopped, and vasopressor support #eaned. :atients shouldalso continue to have their clinical and laboratory parameters ollo#ed closely. These

include blood pressure, arterial lactate, urine output, creatinine, platelet count, Glasgo#coma scale score, serum bilirubin, liver enzymes, o%ygenation +ie, arterial o%ygen tensionor o%yhemoglobin saturation-, and gut unction +table &-. eevaluation is indicated i anyo these parameters #orsen or ail to improve.

$ONT'OL O" T%E SE#TI$ "O$US :rompt identi)cation and treatment o the primary site orsites o inection are essential 26?A=!3. This is the primary therapeutic intervention, #ith mostother interventions being purely supportive. 5ntibiotics should be administered #ithin the )rst si%hours o presentation or earlier.

Identifcation o+ t.e septic +ocus 5 careul history and physical e%amination may yieldclues to the source o sepsis and help guide microbiologic evaluation + table -. 5s an e%ample,sepsis arising ater trauma or surgery is oten due to inection at the site o inIury or surgery. Thepresence o a urinary or vascular catheter increases the chances that these are the source osepsis.

Gram stain o material rom sites o possible inection may give early clues to the etiology oinection #hile cultures are incubating. 5s e%amples, urine should be routinely analyzed viadipstick or leukocyte esterase, Gram stained, and culturedM sputum should be e%amined in apatient #ith a productive coughM and an intraAabdominal collection in a postoperative patientshould be percutaneously sampled under ultrasound or other radiologic guidance.9lood should be dra#n rom t#o distinct venipuncture sites and inoculated into standard bloodculture media +aerobic and anaerobic-. Lor patients #ith a vascular catheter, blood should beobtained both through the catheter and rom another site 2


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o such biomarkers is still in its early stages and should be considered preliminary. "ntiladditional clinical investigations have been perormed, #e do not suggest the routine use o suchbiomarkers to identiy sepsis.

Eradication o+ in+ection :rompt and eJective treatment o the active inection is essential tothe successul treatment o severe sepsis and septic shock 2

4ephalosporin, Drd generation +eg, cetria%oneor ceota%ime- or &th generation+ceepime-, or

9etaAlactamBbetaAlactamase inhibitor +eg, piperacillinAtazobactam,ticarcillinAclavulanate-,or

4arbapenem +eg,imipenemormeropenem-5lternatively, i :seudomonas is a possible pathogen, #e avor combiningvancomycin#ith t#oo the ollo#ing*

5ntipseudomonal cephalosporin +eg, cetazidime, ceepime-, or

5ntipseudomonal carbapenem +eg, imipenem,meropenem-, or

5ntipseudomonal betaAlactamBbetaAlactamase inhibitor +eg,piperacillinAtazobactam,ticarcillinAclavulanate-, or

Lluoro/uinolone #ith good antiApseudomonal activity +eg, ciprofo%acin-, or
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5minoglycoside +eg,gentamicin,amikacin-, or

Konobactam +eg, aztreonam-Selection o t#o agents rom the same class, or e%ample, t#o betaAlactams, should be avoided.@e emphasize the importance o considering local susceptibility patterns #hen choosing anempiric antibiotic regimen.

5ter culture results and antimicrobial susceptibility data return, #e recommend that therapy be

pathogenA and susceptibilityAdirected, even i there has been clinical improvement #hile on theinitial antimicrobial regimen. GramAnegative pathogens have historically been covered #ith t#oagents rom diJerent antibiotic classes. 7o#ever, several clinical trials and t#o metaAanalyseshave ailed to demonstrate superior overall eHcacy o combination therapy compared tomonotherapy #ith a third generation cephalosporin or a carbapenem 2

egardless o the antibiotic regimen selected, patients should be observed closely or to%icity,evidence o response, and the development o nosocomial superinection 21!3. There are nopublished randomized controlled trials testing saety o deAescalation o antibiotic therapy inadult patients #ith sepsis or septic shock 21!D3. The duration o therapy is typically = to 1! days,although longer courses may be appropriate in patients #ho have a slo# clinical response, anundrainable ocus o inection, or immunologic de)ciencies 2=3. 'n patients #ho are neutropenic,antibiotic treatment should continue until the neutropenia has resolved or the planned antibioticcourse is complete, #hichever is longer. 'n nonAneutropenic patients in #hom inection isthoroughly e%cluded, antibiotics should be discontinued to minimize colonization or inection #ithdrugAresistant microorganisms and superinection #ith other pathogens.

Ot.er agents 'nvasive ungal inections occasionally complicate the course o critical illnessin nonAneutropenic patients, especially #hen the ollo#ing risk actors are present* surgery,parenteral nutrition, prolonged antimicrobial treatment, severe sepsis, or multisite colonization#ith 4andida spp. To limit the risk o candidaArelated mortality empirical antiAungal treatmentshave been proposed. 'n a metaAanalysis o studies +most oten comparing fuconazoletoplacebo, but also usingketoconazole,anidulaungin,caspoungin,micaungin,and amphotericin9-, untargeted empiric antiungal therapy possibly reduced ungal colonization and the risk o

invasive ungal inection but did not reduce allAcause mortality 21!&3. Similarly, in a study ocriticallyAill patients ventilated at least )ve days, empiric antiungal treatment +mostlyfuconazole- #as not associated #ith a decreased risk o mortality or occurrence o invasivecandidiasis 21!3. Thus, the routine administration o empirical antiungal therapy is not#arranted in nonAneutropenic criticallyAill patients.

ADDITIONAL T%E'A#IES!lucocorticoids Glucocorticoids have long been investigated as therapeutic agents in sepsisbecause the pathogenesis o sepsis involves an intense and potentially deleterious hostinfammatory response. $vidence rom randomized trials suggest that corticosteroid therapy ismost likely to be bene)cial in patients #ho have severe septic shock +de)ned as a systolic bloodpressure ;

critically ill patients, such as body #eight and midAarm muscle mass. 7o#ever, it is uncertain#hether nutritional support improves important clinical outcomes +eg, duration o mechanicalventilation, length o stay, mortality-, or #hether there is a validated role or speci)csupplements +eg, immune modulators-. The principles o nutritional support in patients #ithsepsis should parallel that in critically ill patients, #hich is revie#ed in detail else#here.Venous t.rom)oem)olism prop.yla0is :atients #ith sepsis and septic shock are atincreased risk or venous thromboembolism such that patients should receivethromboprophyla%is 21!63, the details o #hich are discussed separately.Intensi-e insulin t.erapy 7yperglycemia and insulin resistance are common in critically illpatients, independent o a history o diabetes mellitus 21!=3. The optimal blood glucose range is
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ock-in-adults/abstract/107


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controversial. Kost clinicians target blood glucose levels bet#een 1&! and 1?! mgBdC +=.= to1! mmolBC-. This topic is discussed separately.E0ternal cooling or antipyretics 4ontrolling ever during severe sepsis and septic shockhas potential bene)ts and adverse eJects, the net eJects o #hich are uncertain.5 trial #as perormed to compare the eJects o e%ternal cooling #ith no e%ternal cooling.$%ternal cooling consists o using either an automatic cooling blanket, or iceAcold bed sheets andice packs, to achieve a core body temperature o D6. to D=V4 or &? hours. 't decreases the time

to ever control #ithout e%posing the patient to potential adverse eJects o antipyretic drugs.The trial randomly assigned !! patients #ith septic shock +the patients #ere re/uiringvasopressors, mechanically ventilated, and sedated- to receive either e%ternal cooling or noe%ternal cooling 21!?3. :atients in the e%ternal cooling group had lo#er 1&Aday mortality +1

vasopressors, inotropes, or red blood cell transusions as )rstAline therapy or the restoration otissue perusion +!rade 34-. Therapy should be initiated as early as possible, #ithin si% hours opresentation. Lluid boluses are the preerred method o administration and should be repeateduntil blood pressure and tissue perusion are acceptable, pulmonary edema ensues, or there isno urther response. These parameters should be assessed beore and ater each fuid bolus+See 'nterventions to restore perusionabove.-PLor initial fuid replacement, #e suggest using a crystalloid solution rather than albuminAcontaining solution +!rade 14- and recommend that a hyperoncotic starch solution 0OT beadministered +!rade 3A-. +See 4hoice o fuidabove andQTreatment o severe hypovolemia orhypovolemic shock in adultsQ, section on 4hoice o replacement fuid .-
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PLor patients #ho remain hypotensive ollo#ing intravascular volume repletion, #e recommendvasopressors +!rade 34-M the preerred initial agent isnorepinephrine.+SeeFasopressorsaboveand Q"se o vasopressors and inotropesQ, section on 4hoice o agent in septic shock .-PLor patients #ith severe sepsis and septic shock that are reractory to intravenous fuid andvasopressor therapy, additional therapies, such as inotropic therapy and blood transusions, areadministered based on individual assessment. @e typically reserve red blood cell transusion orpatients #ith a hemoglobin level ;= g per deciliter. +See 5dditional therapiesabove and Q"se o

vasopressors and inotropesQ, section on 4hoice o agent in septic shock .-ULor most patients #ith sepsis and septic shock, #e suggest fuid management be guided usingspeci)c targets +early goalAdirected therapy 2$G(T3-, rather than being managed #ithout speci)ctherapeutic targets. The optimal target to guide fuid management is un5no6n. Lor mostpatients, #e target mean arterial pressure E6 mm7g +calculator 1- and urine outputE!. mCBkgBhour and integrate it #ith static measures o determining ade/uacy o fuidadministration +eg, central venous pressure 24F:3 ? to 1 mm7g-, or dynamic predictors o fuidresponsiveness +eg, respiratory changes in the radial artery pulse pressure- or central venouso%ygen saturation E=! percent. 'n addition, #e ollo# serum lactate +eg, every si% hours-, untilthere is a clear clinical response. +See Goals o initial resuscitationabove.-U:rompt identi)cation and treatment o the site o inection are essential. Sputum and urineshould be collected or Gram stain and culture. 'ntraAabdominal fuid collections should bepercutaneously sampled. 9lood should be taken rom t#o distinct venipuncture sites and romind#elling vascular access devices and cultured aerobically and anaerobically. +See 'denti)cationo the septic ocusabove.-

U5ntibiotics should be administered #ithin si% hours o presentation, preerably ater appropriatecultures have been obtained. @e recommend empiric broad spectrum antibiotics #hen a de)nitesource o inection cannot be identi)ed +!rade 34-. The routine administration o antiungaltherapy is not #arranted in nonAneutropenic patients. +See 5ntimicrobial regimenabove.-U:otentially inected vascular access devices should be removed +i possible-, abscesses shouldbe drained, and e%tensive sot tissue inections should be debrided or amputated + table -.+See $radication o inectionabove.-UGlucocorticoid therapy, nutritional support, glucose control, and investigational therapies areadditional considerations in the management o patients #ith severe sepsis or septic shock. $achis discussed separately.
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