oThe role of the nurse

STAFF EDITOR: MARTHA K. RAYMOND. RN, BSN. BS

HE APPENDECTOMY IS HEALING, though

Mr. Green Still teels weak from the

emergency procedure after his

appendix ruptured. At 70 years old, he

rhought he was in good shape and was man-

.i)',ing his hyperteû^on and type 2 diabetes.

But today, two days after the operation, he

—' feels a little restless as the nurse records

his vital signs. She notes her patient's

temperature is 100.6.'F, heart rate 98 beats

per minute, respirat)&ry rate 22 breaths per

minute, and blood ^ s s u r e 102/76 mm Hg.

His oxygen saturat^n is 95% on room air,

and his weight is sti|>le at 180 lb. Although

the physical assessment is normal, some-

thing tells the nuTseÉiis status is deteriorat-

ing. The nurse revieja the chart to check his

baseline vital signs » i d notes that his tem-

perature and heart ^ t e are elevated, while

his blood pressure a.iSà oxygen saturation are

lower, compared witbthe previous day.

HEATHER DELLACROCE is a Family Nurse Practitioner in awalh-in medical office in Woodbridge, NJ, and works per diem as a criticar ^ ^ ^ ^ ^ ^ ^ ^ ^ _ ^ ^care nurse in îhe trauma critical care unit at the Robert Wood Johnson University Hospital fn New Bfimswickini.

Patients vi/ho have a ruptured appendix riskdeveloping sepsis because pus leaks into theperitoneal space. Mr. Green is at even high-er risk, however, hecause of his advancedage and chronic illness. Not wanting to waitany longer, the nurse calls the surgeon toupdate him on the patient's condition.

WHAT IS SEPSIS? Sepsis is an infection ofthe bloodstream. Tn the US, there are morethan 750,000 new cases of sepsis each year,and the incidence is increasing annually.^The infection tends to spread quickly andoften is difficult to recognize. The mortalityrate associated with severe sepsis remainsunacceptably high—approximately 28% to50%.''' These percentages increase with thenumber of organs affected by the infection,with mortality rates reaching 75% to 85%when four or more organs fail.

Nurses in a variety of settings, fromlong-term care facilities to open-heartcardiac-care units, will care for patientswith severe sepsis. As nurses, we are in aunique position to identify patients at theearliest signs of sepsis and to prevent thespread of severe infection. Early recogni-tion allows for appropriate treatment tobegin sooner, decreasing the likelihood ofseptic shock and the associated cascade oflife-threatening organ failure.

Anyone with an infection may be at risk fordeveloping sepsis, but certain factors mayincrease this risk. The most vulnerablepopulations are the elderly and newhorns;people with chronic illnesses such as diabe-tes or cancer; those who are immunocom-promised, such as after organ transplant,splenectomy, or those with HIV or AIDS;people receiving immunosuppressive ther-apy, such as chemotherapy; and malnour-ished and debilitated patients. •'

PATHOPHYSIOLOGY In order to understandthe body's response to sepsis, we mustfirst review the pathophysiology. Sepsis isa complex process; it is the body's systemicresponse to an infection. When the body isunable to contain a localized infection at itssource, the infecting organism leaks into

the bloodstream, causing sepsis. This is as-sociated with inflammation, coagulopathy,and the maldistribution of blood

When the invading organism, or antigen,enters the bloodstream, it releases endotox-in, a toxic substance usually associated withgram-negative bacteria. In response, thebody's immune system releases proinflam-matory mediators, such as prostaglandinsand cytokines, including tumor necrosisfactor and interleukins, into circulation. ' -^Cytokines are immunomodulators releasedby white blood cells in response to the en-dotoxins, and together they are responsiblefor causing vasodilatation, increased capil-lary permeability, and increased coagula-tion. '* In a healthy person under normalcircumstances, the body can control theseprocesses and heal; but in the septic patient,the endotoxins stimulate the release of toomuch of the immunomodulators, causingan exaggerated, excessive response."*

Vasodilatation is the body's way of increas-ing blood flow to the affected area, therebytransporting more white blood cells, suchas macrophages, to control the originalinfection. However, vasodilatation, withouta proportionate increase in blood volume,leads to hypotension. Increased capillarypermeability allows fluid to leak out of theblood stream and into surrounding tissue,causing edema. This further reduces bloodpressure. Concurrently, fibrinolysis isimpaired leading to a decrease in clotbreakdown. This is thought to he the body'sattempt at confining the antigen.'' How-ever, the formation of fibrin clots leadsto microthrombi, causing hypoperfusionof tissues, tissue necrosis, and eventuallyorgan failure.'*'''

TERMS Although the word "sepsis" is wide-ly used among nurses, it is an extremelycomplex disease with specific diagnosticcriteria. These criteria were established in1991, and revisited again in 2001 at theInternational Sepsis Definitions Confer-ence, a meeting of intensive care expertsfrom around the world. Awareness ofsevere sepsis is low; many septic patients > >

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are under-diagnosed at an early stagewben aggressive treatment could stillreverse tbe course of tbe infection.''Part of the early identification of theseptic patient is understanding theaccepted definitions and criteria fordiagnosing the condition.

Sepsis typically begins witb thesystemic inflammatory responsesyndrome (SIRS), the body's re-sponse to an insult that results in theactivation of the immune response.This inflammatory response is thebody's way of attempting to maintainbomeostasis. Wbile infection is onetrigger for SIRS, tbere are also non-infectious causes, including trauma,burns, myocardial infarction, or in-flammatory processes such as pan-creatitis.** Therefore, it is possible foryour patient to have SIRS witboutbeing septic. SIRS is diagnosed wbenthe patient has two or more of tbefoUowing signs and symptoms: ^

• Body temperature less than 96.8"?(36'C) or above 100.4°F (38'C)

• Heart rate greater than 90 beatsper minute

• Hyperventilation (respir.itory rategreater than 20 breatbs per minute)

• PaCO^ less than 32 mm Hg (nor-mal 35 to 45 mm Hg)

• Wbite blood ceU count greater than12,000/mm' or less than 4,000/mm^(normal 5,000 to 10,000/mm^)"

Sepsis is present when a patient hasSIRS plus a documented infection.Tbis infection can be caused by bacte-ria, viruses, or fungi. Severe sepsisis defined as sepsis complicated byorgan dysfunction, hypotension, orpoor perfusion, and is considered tbemost common cause of deatb in non-coronary critical care units." Signs oforgan dysfunction

• Altered mental status

• Acute oliguria (urine output lessthan 0.5 mL/kg/h)

• Hyperglycemia in the absence ofdiabetes

• Hypoxemia

• Coagulopatby (international nor-malizing ratio (INR) greater than 1.5)

• Gastric ileus -

Hypotension is when the patient'ssystolic blood pressure is less than90 mm Hg or mean arterial pres-sure (MAP) is less than 60 mm Hg.Poor tissue perfusion is evidencedby an increased serum lactate levelor slow capillary refill. Lactic acid isproduced as an end product wbentissues do not receive adequate oxy-gen, resulting in anaerobic metabo-lism. Tberefore, a serum lactate levelgreater than 2 mmol/L is an indica-tor of hypoperfusion and organ dys-function. ' Capillary refill is checkedby applying pressure to the patient'snail bed, causing it to blanch, andthen letting go, counting tbe secondsuntil tbe nail bed turns pink again.Normal capillary refill is less thantwo seconds.

Septic shock is characterized bypersistent bypotension tbat does notimprove even after adequate fluid re-suscitation.** Tbis is evidence of acutecirculatory failure in the septic pa-tient. Fluid resuscitation consists ofcolloids (albumin, packed red bloodcells), crystalloids (normal saline,lactated ringers), or botb. A fluidchallenge may be ordered by the phy-sician if bypovolemia is suspected.This usually consists of 500 mL to1,000 mL of crystalloids or 300 mLto 500 mL of colloids infused over30 minutes.^ At the end of tbe infu-sion, the nurse should reassess the

patient and note any improvementin blood pressure or urine output.Because such a large amount of fluidis infused over a short period of time,the nurse should carefully monitorthe patient for signs of pulmonaryedema, including decreased oxygensaturation and crackles in the lungs.

It is important to note that hypotension in infants and children Is a latesign of septic shock and therefoishould not be used as an indicatorof severe sepsis. Because cbildrenmaintain a higher vascular tonethan adults, blood pressure does not,decrease until tbe cbild is no longable to compensate.'

Looking back at Mr. Green's vitalsigns, we see tbat be meets tbe cri-teria for SIRS (elevated tempernr-'--pulse, and respiratory rate). Bf'of his admitting diagnosis of n ptured appendix, we can presumí 'i*has an infection, fulfilling the LI ,\rria for sepsis. In addition, the nursehad noted the patient was restless,which may be an early indicator otaltered mental status and deteriorat-ing condition. His pbysician ordersblood work, including a completeblood count witb differential, com-plete metabolic panel, arterial bloodgas (ABG), serum lactate, protbrom-bin, and partial tbromboplastintimes, and transfers Mr. Green to theintensive care unit (ICU) for furtherworkup.

MANAGING THE SEPTIC PATIENT In

2003, representatives from 11 inter-national organizations came togeth- jer in an effort to increase awarenessand improve outcomes for patients insevere sepsis. Tbis meeting, known ,1as the Surviving Sepsis Campaign,produced key recommendationsbased upon evidence-based practicefor resuscitating tbe septic patientduring the first six bours after recog-nition of the diagnosis.^

JULY 2009

\

Altered consciou

Confusion

Psyohosis

^rdiovascular

:at'dia

ifhythmias

.. .^potension

.Altered CVP

Respiratory

AnuriarElevated creat'i

Qastrointestinal

iHematologic/hepatic

Elevated liver enzyme;

•Thrombocytopenia

Coagulopathy

Low blood pH

iLn.oreased serum lacta^

SourcM iAlirens T Tuggle D, Surviving severe sepsis: early recognition and treatment, Cnt Care Nurse. October 2004;Suppl:2-13,

Kleinpell RM. Working out the complexities of severe sepsis. Nurse Pract- 2005;30(4):43-48,

Levy MM, Fink MP, Marshall JC, et al. 2001 SCCM/ESICM/ACCPMTS/SIS Internation-al Sepsis Definitions Conference, Cnt Care Med. 2003;31i4):1250-1256,

In Mr, Green's case, the ICU nurseestablishes vascular access to initiateaggressive fluid resuscitation. Becausethe patient arrives with a large bore IVin his arm, this site is used to infusenormal saline. Goals of this initialfluid resuscitation inckftfe increasingthe patient's blood pressure to a MAPgreater than 65 mm Hg and urine out-put-more than 0.5 mL/kg/h,^ In orderto more closely monitor Mr. Green'surine output, the nurse inserts a Foleycatheter with urimeter so that hour-ly measurements may be recorded.Another goal is to maintain a central

venous pressure (CVP) of 8 mm Hg to12 mm Hg/ which can be monitoredby central IV access. CVP is a mea-surement of the pressure of blood en-tering the right side of the heart andis a close estimate of right atrial pres-sure. The benefits of central IV accessinclude having multiple ports throughwhich to infuse fluids and medica-tions, infusion of vasopressors thatcan be irritating to peripheral veins,and the ability to draw blood samplesrather than sticking the patient forvenipuncture.

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"Earlyrecognitiondecreases thelikelihood ofseptic shock andassociated life-threateningorgan failure.

Blood cultures also are ordered to

identify the cause of infection. Cul-

tures should be drawn before start-

ing antimicrobial therapy in order to

most closely identify the organism

causing the sepsis. The administra-

tion of antibiotics prior to drawing

tbe blood cultures may affect the

growth of any pathogen and prevent

a positive culture.^" At least two sepa-

rate cultures should be obtained from

two different sites, with at least one

drawn peripherally.'' When possible,

a culture also should be drawn from

the IV site to determine if the infec-

tion is catheter-related. Once the

cultures are drawn and new vascular

access is obtained, the old IV access

should be promptly removed.^

Next, IV antibiotics should be admin-

istered promptly to improve the odds

ofsurvival.Accordingtotheguidelines.

antibiotics should be administered

within the first hour of the diagnosis

of severe sepsis." The choice of initial

empiric antibiotics should be broad

enough to cover the likely cause of the

infection, and usually includes more

than one type of antibiotic.^ Once

results of the cultures are known, the

antibiotics may be changed to a nar-

rower spectrum to avoid risking the

development of a secondary infection

with resistant pathogens.^

A DOWNWARD SPIRAL Two hours after

arriving in the ICU, Mr. Green's blood

pressure is 88/40 mm Hg with a

MAP of 56 mm Hg even after the ad-

ministration of four liters of normal

saline boluses. Further assessment

reveals hypoactive bowel sounds and

cool, clammy skin. His urine output

for the past two hours has been only

40 mL. Blood work reveals that his

white blood cell count increased from

12.000/mm^ to 30,000/mm^ and

that he has elevated BUN and cre-

atinine, elevated liver function tests,

and an INR of 3.5, which reflect renal

and liver dysfunction. His worsening

hypotension, combined with signs of

organ dysfunction, indicate that the

patient is now in septic shock.

Following unit protocol, a norepi-

nephrine (Levophed) infusion is

started through the central IV cath-

eter. Because Mr. Green's blood pres-

sure has not improved after adequate

fluid resuscitation, guidelines state

that therapy with a vasopressor

should be initiated in order to achieve

minimal perfusion pressure.^

Norepinephrine is a potent vasocon-

strictor and increases blood pressure

without too much change in heart

rate. The goal is to maintain his MAP

above 65 mm Hg, and the nurse ti-

trates the infusion as needed. With

increased perfusion to the kidneys,

his urine output should also improve

with a goal of greater than 0.5 mL/

kg/h. Now that Mr. Green requires

vasopressor therapy, an arterial line

is inserted by the unit physician into

the patient's radial artery in order to

closely monitor his blood pressure.

Vasopressin (Pitressin) is another va-

soconstrictor that is commonly used,

often in conjunction with norepi-

nephrine, to maintain adequate per-

fusion pressure. Doses of vasopressin

should not exceed 0.04 units/min, as

this has been associated with myo-

cardial ischemia and cardiac arrest.^

The guidelines also suggest the ad-

dition of an inotrope, or medication

that increases the force of the heart's

contraction, in order to increase car-

diac output and improve tissue per-

fusion. Dobutamine (Dobutrex) is

the first-choice inotrope for patients

with low cardiac output that does not

improve with fluid resuscitation,^

Four hours after Mr. Green's admis-

sion into the ICU, the nurse notices

that he is becoming more restless and

his breathing appears labored at 34

breaths/min. His oxygen saturation

20|nM|J' 2009

now is only 89% on supplemental oxy-gen. Upon auscultation, the nurse notescrackles in his lungs to both lower lobes.An ABG reveals pH 7.26 (normal 7.35to 7.45), PaCO^ at 51 mm Hg (normal35 mm Hg to 45 mm Hg), PaO^ at 60mm Hg (normal 80 mm Hg to 100 mmHg) and HCO3 at 24 mEq/L (normal 22mEq/L to 28 mEq/L), indicating respira-tory acidosis and hypoxemia. In addition,his serum iactate is 4.5 mmol/L.

As the downward spiral of septic shockprogresses, the capillary permeabilitycontinues to increase, which interfereswith gas exchange across the alveo-larcapillary membrane.'' Mr. Green isintubated and placed on mechanicalventilation to facilitate oxygen deliveryand reduce the work of breathing. Thenurse starts an IV infusion of midazol-am (Versed) and fentanyl (Sublimaze)to keep the patient comfortable. Othernursing interventions include care ofthe endotracheal tube to maintainpatency and suction as needed, oralcare with chlorhexidine rinse, andmaintaining the head of the bed at45 degrees, which has been shownto reduce the incidence of ventilator-acquired pneumonia.'''^

After the initial stabilization of thepatient, ICU nurses continue to monitorthe patient's condition carefully, record-ing vital signs on an hourly basis, mea-suring intake and output, titrating hisdrips, and administering his medica-tions as ordered. After consulting withthe nutritionist, the physician orderscontinuous total parenteral nutrition(TPN) until the patients bowels becomefunctional again.

A continuous infusion of insulin also isstarted to maintain blood glucose valuesless than 150 mg/dL, which has beenshown to significantly improve survivalin surgical patients.-' The nurse moni-tors Mr. Green's blood sugars hourly un-til stable, and then on a regular basis, atleast every four hours. Because the need

for vasopressor therapy indicates adrenalinsufficiency, the patient is given IV hy-drocortisone (A-Hydrocort, Solu-Cortef).This also has been shown to reduce mor-tality rates in patients in septic shock.

One of the last treatment options forpatients considered at high risk forsepsis-related death is therapy withdrotrecogin alfa (activated) (Xigris).This is a recombinant form of human-activated protein C, or rhAPC, a natu-rally occurring protein made by thebody with both anticoagulant and anti-inflammatory properties.

As sepsis progresses, levels of activatedprotein C decrease in the body, lead-ing to increased clotting and thereforeworsening tissue ischemia.* The rhAPChas been shown to improve survival inpatients with sepsis-induced organ dys-function, and guidelines state it shouldbe given as soon as possible once thepatient is identified as being at highrisk of death.'-' Because drotrecogin alfa(activated) may potentially increase therisk of bleeding, it may be contraindi-cated in some patients, and the risksand benefits should be weighed for eachindividual patient.

POSITIVE OUTCOME As a last resort, Mr.Green is started on drotrecogin alfa (ac-tivated). Eight hours later, his vital signsand lab values begin to improve. His el-evated white blood cell count begins tocome down, and liver and renal functiontests also begin to trend down. Urineoutput also improves. Over the nextseveral days, he is able to be weaned offvasopressors and continues to maintainadequate blood pressure. After a sponta-neous breathing trial, Mr. Green is extu-bated and placed on a nasal cannula foroxygen delivery. As his bowel functionreturns, he is started on enterai nutri-tion and begins to regain his strength.Four days later, he is transferred out ofthe ICU and back to the medical/surgicalunit, where he continues to make prog-ress before being discharged home.

This success story might not havebeen possible without the sharpassessment skills of Mr. Green'snurses. One of our roles as a nurseis that of patient advocate, and assuch we are closest to the patient,placingus in akey position to iden-tify any subtle changes at theirearliest onset. Knowledge of thesigns and symptoms of SIRS, sep-sis, and septic shock is key to thisearly recognition. Once sepsis isdiagnosed, early and aggressivetreatment in accordance with theSurviving Sepsis Campaign guide-lines can begin, which greatlyreduces mortality rates associatedwith sepsis.^ ! • •

References

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2. Ahrens T, Tuggle 0. Surviving severesepsis; Early recognition and treatment.Cni Care/Vüße. October 2004;Suppl:2-I3.

3. Robson W, Newell J. Assessing,treating, and managing patients witbsepsis. Nurs Stand. 2005;I9(50);56-64.

4.WoodS, LavieriMCDurkinT.What you need to know about sepsis.J V > ^ ( 7 ? 7 2 0 0 7 3 7 3

5. Bridges EJ. Dukes S. Cardiovascularaspects of septic shock; pathophysiol-ogy, monitoring, and treatment. CritC A ' 2 0 0 5 2 5 2

6, Kleinpell RM. Working out thecomplexities of severe sepsis.A'üreePracf.2Q05;30(4):43-48.

7.KumarV, CotranRS, RobbinsSLffobbins Baste Pathology. 7th ed.Philadelphia. PA; Saunders; 2003.

8.LevyMM,FinkMP, MarshailJCetal.2001 SCCM/ESICM/ACCPMTS/SIS Inter-national Sepsis Definitions Conference.Cnf Care Werf. 2003;31(4);1250-1256.

9. Dellinger RP, Carlet JM, Masur H. et al.Surviving Sepsis Campaign guidelines formanagement of severe sepsis and septicshock. Crit Care Mea. 2004;32(3):858-873.

10. Vandijck DM, Bfot SI. Decruyenaere JM.Update on the management ot infectionin patients with severe sepsis. DimensCht Care Nurs. 2008;27(6)744-248.

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