sepsis

sepsisToday is the fourth admission in a monthfor Mr. Hammill, 70, who has a recent med-ical history of coronary artery bypass graftsurgery and atrial fibrillation and also ahistory of coronary artery disease, chronicobstructive pulmonary disease, diabetes,gastroesophageal reflux disease, anemia,and anxiety. Well known to you as an inter-active and communicative man, you findthat during this admission he’s irritable andless talkative. You also note that he has gen-eralized edema, coarse rhonchi in the ante-rior lobes, and crackles in the bases of bothlungs, and he’s coughing up tan-coloredsputum. This morning, he’s confused uponawakening, and throughout the course ofthe day you need to reorient him to his sur-roundings.

His ability to answer questions correctlyearlier in your shift suddenly declines. He’stachypneic with a respiratory rate of 32breaths/minute, an irregular pulse, and aheart rate of 110 beats/minute. His serumlactate level is 12 mmol/L. What’s going onwith Mr. Hammill? The healthcare team sus-

40 Nursing made Incredibly Easy! May/June 2009

2.5ANCC

CONTACT HOURS

Sepsis is the number onecause of death in the ICU, the10th leading cause of deathworldwide, and the 11th leadingcause of death in the UnitedStates. Older patients withchronic illnesses are at highrisk for developing this condi-tion. We discuss what you needto know about sepsis and yourrole in caring for a patient whohas it. By Margaret J. McCormick, RN, MSClinical Assistant ProfessorTowson University • Towson, Md.

The author has disclosed that she has no significant relationshipswith or financial interest in any commercial companies that pertainto this educational activity.

Recognizing the signposts for

sepsis

May/June 2009 Nursing made Incredibly Easy! 41

pects sepsis on the basis of his age and clini-cal findings.

To start, let’s review what sepsis is andhow it evolves.

Sepsis = seriousA systemic inflammatory response to thepresence of infection (such as Gram-positiveor Gram-negative bacteria, fungi, viruses,mycobacteria, or parasites) that canprogress to circulatory systemic dysfunc-tion, multiple organ failure, and death, sep-sis is a complex disease process that carries

a high degree of morbidity and mortality.Older patients are at increased risk for

sepsis and it may be more difficult todiagnose clinically in this age group.Babies and immunocompromisedpatients are also at increased risk.

The incidence of sepsis is reported asthree cases per 1,000 people; in hos-pitalized patients, the incidence is 2%.

The rise in sepsis cases is believed to berelated to the growing number of im-

munocompromised patients, a greaternumber of invasive procedures being

performed in the ICU, an increased numberof resistant organisms, and a rise in thenumber of older patients with critical ill-nesses.

What are the events that can lead to sep-sis? Let’s find out.

A complex cascadeInflammation is the body’s response to in-sults that arise from chemical, traumatic, orinfectious stimuli. The inflammatory cascadeis a complex process that involves humoraland cellular responses and complement andcytokine cascades (see A complex cascade).What does this mean? Following an insult tothe body, local cytokines are produced andreleased into the circulation to promote a lo-cal response. Growth factor stimulation andrecruitment of macrophages and plateletsoccur. The goal is homeostasis; however, ifhomeostasis doesn’t occur from the local re-sponse to inflammation, the result is a sys-


If I breakthrough your

patient’sdefenses,

sepsis mayresult.

A complex cascade

Activatedprotein C

Endothelium

Tissue factor

Tissue factor

Monocyte

Inhibition

InhibitionPathogens and

endotoxin

Inflammatoryresponse to infection


Activatedprotein C

Coagulation cascade

Factor VIIIa

Fibrin

Thrombin-activatablefibrinolysis inhibitor

Limitsadhesion

Inactivation

InactivationPreventsactivation

Plasminogenactivator

inhibitor-1

Fibrin clot

Factor Va

Thrombin

Neutrophil

Proinflammatorycytokines:

Interleukin-6

Interleukin-1

Tumor necrosisfactor-alpha

Tumor necrosisfactor-alpha

Interleukin-1

Activatedprotein C

Activatedprotein C

Inactivation

Fibrinolytic responseto infection

Thrombotic responseto infection

temic inflammatory reaction.The most prominent systemic manifesta-

tion of inflammation is known as the acutephase response. This constellation of sys-

temic effects usually begins within hoursor days of the onset of inflammation.The release of cytokines, such as inter-leukin (IL)-1, IL-6, and tumor necrosisfactor (TNF), causes the thermoregula-

tory center in the hypothalamus toproduce an elevation in the

patient’s body temperature,resulting in a fever. During theacute phase response, the

bone marrow produces moreimmature neutrophils and the

liver increases fibrinogen and C-reactiveprotein production. Skeletal muscle catabo-lism provides amino acids that can be usedin the repair of tissue. IL-8 may perpetuatetissue inflammation. IL-6 and IL-10 aug-ment the acute phase response by generat-ing additional proinflammatory mediators.

The unregulated release of proinflamma-tory mediators or cytokines can elicit toxicreactions and promote endothelial cell-leukocyte adhesion, releasing cell-damagingproteases and prostaglandins, which partici-pate in the generation of fever, tachycardia,ventilation/perfusion abnormalities, and lac-tic acidosis, and activating the clotting cas-cade. Endotoxins cause tissue damage byreleasing prostaglandins, and the resultingvasodilation and increased capillary perme-ability allow fluid to enter the interstitialspace, causing edema and hypotension. Thelack of oxygen at the cellular level causes therespiratory system to fail, followed by renal,gastrointestinal (GI), and liver failure.Platelet aggregation and thrombi formbecause of the increased viscosity of theblood. This can result in decreased tissueperfusion and the development of dissemi-nated intravascular coagulation (DIC), oridiosyncratic bleeding and clotting. This canultimately lead to multiple organ damageand dysfunction.

Pinning down the culpritSepsis can occur in people of all ages, but it’smore prevalent in older patients. In one na-tionwide study, it was found that patientsolder than age 65 accounted for 64.9% of allsepsis cases. A possible reason for this highincidence is the fact that older patients aremore likely to have Gram-negative infec-tions, particularly associated with pneumo-nia, and comorbid conditions. Possiblecauses of sepsis include:• pneumonia • urinary tract infection (UTI)• diarrhea or distension• meningitis• cellulitis


Here’s a handycheat sheet

with definitionsgalore.

Important definitionsBacteremia: the presence of bacteria in the blood.Infection: the presence of microorganisms that trigger an inflam-matory response.Hypotension: a systolic BP of less than 90 mm Hg or a drop insystolic BP of greater than 40 mm Hg from the patient’s baselineBP.Sepsis: a systemic response to infection; may occur after a burn,surgery, or serious illness and is manifested by two or more clinicalsigns and symptoms:• temperature greater than 100.4° F (38° C) or less than 96.8° F (36° C)• heart rate of greater than 90 beats/minute• respiratory rate of greater than 20 breaths/minute• partial pressure of carbon dioxide level of less than 32 mm Hg• WBC count greater than 12,000 cells/mm3, less than 4,000 cells/mm3,or greater than 10% immature WBC (bands)• hyperglycemia and abnormal clotting and bleeding.Severe sepsis: the presence of signs and symptoms of sepsis-relatedorgan dysfunction, hypotension, or hypoperfusion; clinical signs andsymptoms include those of sepsis as well as:• lactic acidosis• oliguria• thrombocytopenia• altered level of consciousness.Septic shock: shock associated with sepsis; characterized by symptomsof sepsis plus hypotension and hypoperfusion despite adequate fluid vol-ume replacement.SIRS: a syndrome resulting from a severe clinical insult that initiates anoverwhelming inflammatory response by the body.MODS: the presence of altered function of one or more organs in anacutely ill patient requiring intervention and support of the organs toachieve physiologic functioning required for homeostasis.

sheet

cheat

• septic arthritis• wound infection• endocarditis• catheter-related infection.

Sepsis may start with systemic inflamma-tory response syndrome (SIRS). The diagno-sis of SIRS requires two or more of the fol-lowing clinical findings: • body temperature of greater than 100.4° F(38° C) or less than 96.8° F (36° C)• heart rate of greater than 90 beats/minute• respiratory rate of greater than 20breaths/minute or a partial pressure of car-bon dioxide measurement of less than 32mm Hg • white blood cell (WBC) count of greaterthan 12,000/mm3 or less than 4,000/mm3 orgreater than 10% immature forms of neu-trophils or bands.

A patient with systemic manifestations ofinfection plus a documented infection hassepsis. A patient with sepsis complicated byorgan dysfunction, tissue hypoperfusion (anelevated serum lactate level or oliguria), orsepsis-induced hypotension (a systolic BP ofless than 90 mm Hg or a mean arterial pres-sure [MAP] of less than 70 mm Hg, or adecrease in systolic BP of greater than 40 mmHg below normal for the patient’s age in theabsence of other causes) has severe sepsis. Apatient with sepsis-induced hypotensionthat persists despite adequate fluid resuscita-tion and isn’t explained by other causes hasseptic shock.

Complication stationComplications associated with sepsis in-clude acute respiratory distress syndrome(ARDS), acute renal failure, GI complica-tions, DIC, and multiple organ dysfunctionsyndrome (MODS). Let’s take a closer look.

ARDS is defined as the abrupt onset ofrespiratory distress accompanied by threecomponents: severe hypoxemia, bilateralpulmonary infiltrates seen on X-ray, and theabsence of heart failure or fluid overload.Hypoxemia may be present before the onsetof other clinical signs. Tachypnea and tachy-

cardia are seen during the first 12 to 24hours, followed by a dramatic increase inthe work of breathing. The three phases ofARDS are the acute exudative phase, whichis characterized by profound hypoxemia andassociated with inflammation and diffusealveolar damage; the fibroproliferativephase, which is associated with decreasedcompliance and increased dead space; andthe resolution phase, which may take 6 to 12months or longer to resolve.

Acute renal failure may develop as aresult of endotoxins, which are powerfulvasoconstrictors that can cause intravascular


Signs of acute organsystem failureCardiovascular

• Tachycardia• Arrhythmias• Hypotension• Elevated central venous and pulmonaryartery pressures

Respiratory

• Tachypnea• Hypoxemia

Renal

• Oliguria• Anuria• Elevated creatinine

Hematologic

• Jaundice• Elevated liver enzymes• Decreased albumin• Coagulopathy

GI

• Ileus (absent bowel sounds)

Hepatic

• Thrombocytopenia• Coagulopathy• Decreased protein C levels• Increased D-dimer levels

Neurologic

• Altered consciousness• Confusion• Psychosis


Common medications used to treat sepsisClassification of drug Indications Nursing care

Isotonic crytalloids

0.9% sodium chloride Used for fluid resuscitation Monitor cardiac, renal, and pulmonary function; solution watch for edema in the extremities and signs of

changes in mental status

Lactated Ringer’s Used for fluid resuscitation Monitor hemodynamic responsesolution

Colloids

Albumin 5% Used for volume expansion May exacerbate renal insufficiency

Antibiotics

Cefotamine Used for Gram-negative coverage against Adjust dose in severe renal failureEscherichia coli and Proteus, Klebsiella,and Pseudomonas species

Ceftriaxone Used because of increased prevalence of Adjust in renal impairment; use caution if the patient penicillinase-producing microorganisms is allergic to penicillin

Cefuroxime Used for Gram-positive coverage against Monitor renal function; administer a half dose if E. coli, Klebsiella peneumoniae, Proteus creatinine clearance is 10 to 30 mL/minutemirabilis, and Haemophilus influenzae

Ticarcillin Used as an antipseudomonal penicillin Monitor renal function and adjust dosage in patients and beta-lactamase inhibitor with severe colitis

Clindamycin Used against anaerobes (may have some Monitor PT, digoxin, and theophylline levelsactivity against streptococcus and methicillin-sensitive S. aureus)

Metronidazole or Used against Gram-positive and aerobic Metronidazole can potentiate warfarin; ciprofloxacin ciprofloxacin Gram-negative organisms in GI infections and may increase digoxin and theophylline levels

infectious diarrhea

Activated protein C analogues

Drotrecogin alfa Used for severe sepsis with acute organ Monitor for hypersensitivity; contraindicated if the dysfunction patient is at increased risk for bleeding, has had a

recent stroke, or has head trauma, has an epidural catheter, or is on heparin therapy

Vasopressors

Dopamine Used to treat hypotension in fluid Hemodynamic effects are dose related; monitor resuscitated patients; stimulates adrenergic urine output, cardiac output, pulmonary wedge pres-and dopaminergic receptors sure, and BP.

Norepinephrine Used to treat hypotension following fluid Use in caution in patients with occlusive vascular volume replacement; stimulates beta1- disease; correct blood volume depletion before adrenergic and alpha-adrenergic receptors administration; extravasation may result in severe and increases cardiac contractility tissue necrosis

Vasopressin Increases vasomotor tone in patients with Dosage is one-tenth of what’s used to treat an upper septic shock; also increases water reabsorption GI bleed from esophageal varices; monitor BP and at the distal renal epithelium and promotes urine outputsmooth muscle contraction throughout the vascular bed of the renal tubular epithelium

clotting. The degree of renal damage is rela-tive to the severity and duration of theshock. Acute tubular necrosis may occurbecause of severe ischemia to the kidneys.With careful monitoring of urine output andserum creatinine and blood urea nitrogenlevels, acute renal failure is reversible.

GI complications can develop whenthere’s a redistribution of blood flow to themucosal layer of the GI tract. Superficiallesions can cause stress ulcers in the stom-ach. Bleeding is a common symptom, andhemorrhage can occur 2 to 10 days after theinsult.

DIC is caused by activation of the coagula-tion cascade, resulting in the formation offibrin clots and thrombotic occlusion of smalland midsized vessels. The delayed removalof fibrin occurs because of impaired fibrinol-ysis. Depletion of platelets and coagulationfactors increase the risk of bleeding. Fibrindeposits in organs can cause ischemic dam-age and organ failure.

MODS occurs when multiple organs, suchas the kidneys, liver, lungs, brain, and heart,are damaged as a consequence of septicshock. The mortality rate increases with thenumber of failing organs. See Signs of acuteorgan system failure for more information.

Lab tests at the readyEarly detection of sepsis is critical so thatappropriate intervention can be imple-mented. Aggressive treatment protocolshave been shown to decrease mortalityrates by 30% for severely septic patients andby 50% for patients who haven’t yet devel-oped the disease.

Lab tests to diagnose sepsis include:• metabolic studies, including evaluation ofserum electrolyte levels. Often patients withsepsis have hypocalcemia, hyper- or hypo-glycemia, an elevated blood urea nitrogenlevel, and mild hyperbilirubinemia.• complete blood cell (CBC) count with dif-ferential and platelet count. An adequatehemoglobin level (7 to 9 g/dL for adults) isnecessary to ensure oxygen delivery in

patients with septic shock. Platelets are acutephase reactants and usually rise at the onsetof any serious stress. The platelet count willfall with persistent sepsis. An elevated WBCcount may predict bacterial infection. Thepatient may have leukocytosis, leukopenia,azotemia (an accumulation of nitrogenouswaste products in the blood), thrombocy-topenia, anemia, or hypoxemia.• coagulation studies. Assess prothrombintime (PT) and partial thromboplastin time.Patients with sepsis often have a prolongedPT time. Patients with clinical evidence ofcoagulopathy require additional tests todetect the presence of DIC. • arterial blood gas (ABG) analysis.Measure serum lactate levels to assess tissueperfusion. An elevated serum lactate level(above 4 mmol/L) indicates significant tissuehypoperfusion and a shift from aerobic toanaerobic metabolism. In severe cases, thepatient may have lactic acidosis.• cultures of sputum, urine, cerebrospinalfluid, wound drainage, or respiratory secre-tions. Tissue Gram staining from the site ofthe possible infection can provide guidancein the choice of antibiotic therapy. A spu-tum culture can determine the presence ofpneumonia; a urine culture can determinethe presence of UTI.

How’s sepsis treated? That’s up next.

Bundle upAccording to the Surviving Sepsis Cam-paign’s guidelines for the management ofsevere sepsis and septic shock, using a sep-sis bundle can reduce mortality in severecases. A bundle is defined as a group of in-terventions related to a disease process that,when implemented together, result in betteroutcomes than when implemented individ-ually. Treatment for sepsis includes the fol-lowing six interventions: • give 100% oxygen via non-rebreathermask. Because the metabolic demands foroxygen are massively increased in sepsis,the need for intubation and mechanical ven-tilation may be required if ABG levels dete-


Septic shockcan damage

all of us?Yikes!

riorate and blood pH decreases. • obtain two separate blood cultures beforeantibiotic therapy is initiated. At least twoblood cultures should be drawn before an-tibiotic therapy initiation, with at least onedrawn percutaneously and one drawnthrough each vascular access device, unlessthe device was recently inserted (less than48 hours). Source control is also an impor-tant strategy for certain types of sepsis pa-tients. Recent studies done on patients withsepsis show that removing any infected de-vice and debriding necrotic or infectious tis-sue, especially in skin and soft tissue infec-tions, are recommended. Drainage anddebridement may also be appropriate forpatients with empyema (the collection ofpus within an anatomic cavity), sinusitis,and infections of the chest and medi-astinum. • initiate antibiotic therapy. Because sepsisis caused by an infectious disease, one ofthe cornerstones of patient management isantibiotic therapy. The appropriateness andtiming of antibiotic coverage is important.Initially, a broad-spectrum antibiotic shouldbe used, with emphasis on the most likelypathogens, but should be discontinuedwithin 3 to 5 days. Antibiotic therapy ismodified after cultures are available and an-tibiotic susceptibility patterns are known.Single antibiotic therapy may last for 7 to 10days and in certain cases may be longer,such as in patients with a slow response,those who are immunologically deficient,or those with an area of infection that’sundrainable. Dosage adjustments may bebased on renal function. • initiate fluid resuscitation. Another cor-nerstone of treatment is the infusion of I.V.fluid to restore the circulating volume lostas fluid leaks from capillaries. Crystalloidsolutions, such as 0.9% sodium chloride orlactated Ringer’s solution, or colloids, suchas albumin, will help to keep the MAPabove 65 mm Hg. Wedge pressure shouldbe maintained at 6 to 12 mm Hg; central ve-nous pressure, 8 to 12 mm Hg; and sys-

temic vascular resistance at 800 to 1,200dynes/sec/cm-5 The typical amount ofcrystalloid solution for both severe sepsisand septic shock ranges from 4 to 8 liters.Fluid challenges with 300 to 500 mL of crys-talloids or colloids may be given based onBP and urine output. This extra fluid willhelp blood flow to the organs. Careful mon-itoring is necessary to prevent overload in apatient with known heart failure.• measure the patient’s lactate and hemo-globin-A lactate levels. Septic shock is diag-nosed when the lactate level is greater than4 mmol/L in the presence of severe sepsis.A low hemoglobin value means that theamount of oxygen carried to the organs andtissue is reduced. If the hemoglobin level isless than 7 g/dL, a blood transfusionshould be considered. • insert a urinary catheter to monitorhourly urine output. Urine output is a goodindicator of how well the patient’s kidneysare being perfused. If the amount of urinedrained by the catheter is low, it couldmean that circulation to the body is im-paired and fluid challenges are needed torestore perfusion.

Now let’s delve deeper into antibiotictherapy and other medications used to treatsepsis (see Common medications used to treatsepsis).

Meds up to batAccording to the guidelines, antibiotic ther-apy should be started within the first hour,if possible. A recent study examined thetiming of antibiotic therapy and found thatevery additional hour without effective an-tibiotic therapy can increase the risk ofdeath in patients with hypotensive sepsisby 7.6% during the first 6 hours. The choiceof antibiotic prescribed by the healthcareprovider depends on complex issues relatedto the patient’s history, drug intolerances,underlying diseases, clinical syndromes,and susceptibility patterns of pathogens inthe community and hospital. Cliniciansshould be cognizant of the virulence and


Antibiotics areimperative for

the patientwith sepsis.

I’m alwayslooking for a

way in...


growing prevalence of methicillin-resistantStaphylococcus aureus infection and the pos-sibility of candidemia when choosing ap-propriate antibiotic therapy. It’s recom-mended that patients with severe sepsisreceive broad-spectrum antibiotic therapyuntil the causative organism and antibioticsusceptibilities are found. Although appro-priate cultures need to be obtained beforestarting antibiotics, it shouldn’t delay ther-apy. Premixed antibiotics or bolus antibi-otics may facilitate prompt administration.

Vasopressors, such as dopamine and nor-epinephrine, are used to restore tissue perfu-sion pressure. Dopamine increases myocar-dial contractility and is more likely toincrease cardiac output; however, it mayincrease the patient’s heart rate and producetachyarrhythmias. Norepinephrine is a morepotent vasoconstrictor and has been found tobe more effective than dopamine in restoringhemodynamic stability. It’s considered tobe a first-line choice of drug therapy forpatients with sepsis. The use of vasopressinwas recently studied in the Vasopressin andSeptic Shock Trial. During this study, it wasfound that patients requiring vasopressors(norepinephrine or vasopressin) for at least 6hours who had one dysfunctional organ sys-tem had no difference in 28-day survival.

The use of corticosteroids may be helpfulto decrease complement activity, plateletactivation, TNF, and proinflammatorycytokines. Guidelines state that the use ofcorticosteroids is indicated for adult patientswith septic shock when hypotension remainspoorly responsive to adequate fluid resusci-tation and vasopressors.

Drotrecogin alfa was approved for use bythe FDA in 2001 for the treatment of severesepsis. This recombinant form of human acti-vated protein C is the first of a new categoryof medications that act on the body’s re-sponse to infection at the level of the bloodvessel. The inflammatory cascade that occursduring severe sepsis causes activation of thecoagulation system associated with impairedfibrinolysis. This can result in changes in the

microvasculature circulation associated withmultiorgan dysfunction and death. Trialsshow that the use of drotrecogin alfa reducesthe risk of death among patients with severesepsis by 20% because it inhibits thrombosisand inflammation and promotes fibrinolysis.It also prevents microvascular dysfunctionand coagulation, improves tissue perfusionand oxygenation, and reverses hypotension.Drotrecogin alfa is recommended forpatients with severe sepsis or septic shockwho are at high risk for death. Patients con-sidered for treatment should be carefullyevaluated. Due to its antithrombolytic effect,this drug is contraindicated if the patient isexperiencing active internal bleeding; hashad recent head trauma, GI bleed-ing, or surgery; or has anepidural catheter in place. Andit shouldn’t be given 2 hoursbefore an invasive or surgicalprocedure. Recently, the FDAhas issued a label warningabout administering drotrecoginalfa to patients with single organdysfunction who have recentlyundergone surgery or those who maynot be at high risk for death.

The role of the nurse will beplayed by…What should you do when caring for a pa-tient with sepsis?

Nursing interventions include:• infection control measures. It’s criticalthat you strictly follow infection controlmeasures, including practicing proper handhygiene as outlined by the CDC.• assessment and monitoring. Assess anddocument the patient’s vital signs at leastevery hour. Monitor body temperature,respiratory rate, BP, MAP and central ve-nous pressure, heart rate, urine output,and oxygen saturation values. Lab moni-toring of a patient’s blood glucose level isrecommended every 30 to 60 minutes be-cause tight glycemic control (under 150mg/dL) has been shown to improve out-

comes. Frequently perform neurologicchecks to assess any change in mental sta-tus. Monitor for coagulation abnormalities.If the patient starts oozing or bleedingfrom three separate sites (such as the nose,a wound, and the I.V. site) or has petechiaeor cyanosis, he may be developing DIC.Also be alert for the presence of cold, mot-tled, or cyanotic extremities because a mi-crovascular occlusion forms clots to distaltissues. Report these findings to the health-care provider.• proper documentation. Documentation

should include the following: the type ofrespiratory support and results of ABG

analysis, the type and location of I.V.access, and the time and amount ofI.V. crystalloids, colloids, antibiotics,or vasopressors given. Report anddocument results of lab tests such asthe CBC count; electrolyte, blood glu-

cose, and lactate levels; and coagulationstudies. • communication with the patient’sfamily. Families of patients with sep-

sis may feel helpless during this criticaltime. They need frequent explanations of

interventions and procedures, as well ascompassionate care. Communication aboutend-of-life issues and life-sustaining mea-sures ahead of time allows the family to un-derstand what’s happening to their lovedone and make informed choices and deci-sions.

On the road to recoverySo what’s happening with our patient, Mr.Hammill?

Mr. Hammill’s condition is medicallycomplex and he’s critically ill. His WBCcount is 25,000/mm3 and sputum culturesidentify the source of sepsis as pneumonia.Mr. Hammill is placed on a broad-spectrumantibiotic. Over the course of the day, hebecomes more confused and then obtunded.His oxygen saturation value falls to 85% andhe becomes acutely hypotensive. He’s resus-citated and placed on mechanical ventila-

tion. Despite the administration of I.V. flu-ids, he remains hypotensive. He’s started onvasopressors in an attempt to maintain aMAP of greater than 65 mm Hg. His urineoutput from the indwelling catheter drops to10 mL/hr. He’s given additional I.V. colloidsand a total of 200 mL of albumin. Later thatnight, his condition begins to improve.

Signposts aheadSepsis is a significant cause of morbidityand mortality in older patients. The diagno-sis of sepsis can be particularly difficult inthis age group, and a high index of suspi-cion is necessary for early identification andintervention. Deterioration in the clinicalcondition of an older patient may be subtleand easily missed, so each encounter mayprovide clinical clues that can alert you tochanges in physiologic status, which maybe an early manifestation of sepsis. By un-derstanding the signposts for sepsis, you’llbe able to recognize and rapidly identify apatient developing this condition so thatimmediate and appropriate managementcan be implemented. n

Learn more about itDellinger RP, Levy MM, Carlet JM, et al. Surviving SepsisCampaign: international guidelines for management of se-vere sepsis and septic shock: 2008. Crit Care Med. 2008;36(1):296-327.Dombrovskiy V, Martin A, Suderram J, Paz H. Use ofdrotrecogin alpha (activated) for severe sepsis in NewJersey acute care hospitals. Am J Health Syst Pharm.2006;63(12):1151-1156.Domino FJ. The 5 Minute Clinical Consult. 17th ed.Philadelphia, PA: Lippincott Williams & Wilkins; 2008.Kumar A, Roberts D, Wood KE, et al. Duration of hy-potension before initiation of effective antimicrobial ther-apy is the critical determinant of survival in human septicshock. Crit Care Med. 2006;34(6):1589-1596. Martin GS. SAFE, VASST, LIPOS Trial 3, CORTICUS andmore: implications for the Surviving Sepsis Campaignguidelines. http://www.medscape.com/viewarticle/555167.Picard KM, O’Donoghue SC, Young-Kershaw DA, RussellKJ. Development and implementation of a multidiscipli-nary sepsis protocol. Crit Care Nurse. 2006;26(3):43-54.Porth CM. Essentials of Pathophysiology: Concepts of AlteredHealth States. Philadelphia, PA: Lippincott Williams &Wilkins; 2004:334-335.Porth CM. Pathophysiology: Concepts of Altered HealthStates. 7th ed. Philadelphia, PA: Lippincott Williams &Wilkins; 2006:387-401.


Early ID ofdevelopingsepsis andimmediate

managementare key.

Robson WP, Daniel R. The sepsis six: helping patients tosurvive sepsis. Br J Nurs. 2008;17(1):16-21.Sakr Y, Reinhart K, Vincent JL, et al. Does dopamine ad-ministration in shock influence outcome? Results of theSepsis Occurrence in Acutely Ill Patients (SOAP) study.Crit Care Med. 2006;34(3):589-597. Sharma S, Eschun G. Multisystem organ failure of sepsis.

http://www.emedicine.com/MED/topic3372.htm.Smeltzer SC, Bare BG, Hinkle JL, Cheever KH. Brunnerand Suddarth’s Textbook of Medical-Surgical Nursing. 11thed. Philadelphia, PA: Lippincott Williams & Wilkins;2007:373.Strategies for Managing Multisystem Disorders. Philadelphia,PA: Lippincott Williams & Wilkins; 2005:326-329.


On the WebThese online resources may be helpful to your patients and their families:• eMedicine Health: Sepsis (blood infection): http://www.emedicinehealth.com/sepsis_blood_ infection/article_em.htm• Mayo Clinic: Sepsis: http://www.mayoclinic.com/health/sepsis/DS01004• Medline Plus: Sepsis: http://www.nlm.nih.gov/medlineplus/sepsis.html• Sepsis.com: http://sepsis.com/index.jsp• Surviving Sepsis Campaign: http://www.survivingsepsis.org.

Earn CE credit online: Go to http://www.nursingcenter.com/CE/nmie and receive a certificate within minutes.

For more than 38 additional continuing education articles related to infection, go to Nursingcenter.com/CE.

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1. Which statement most accurately describes sepsis?a. It’s a severe infection complicated by tissue hypoperfusion.b. It’s a systemic inflammatory response to the presence of

infection. c. It’s an infection-induced hypotensive state that doesn’t re-

spond to fluid resuscitation.

2. The inflammatory cascade involves all of the followingexcepta. production and release of local cytokines into the circulation.b. inhibition of macrophages and platelets.c. release of tumor necrosis factor.

3. Multisystem failure (respiratory, renal, GI, and liver) inshock is due to a. lack of oxygen at the cellular level.b. decreased capillary permeability.c. intravascular fluid overload.

4. Which isn’t a clinical sign of systemic inflammatoryresponse syndrome?a. white blood cell count of 3,800 mm3

b. temperature of 96.2° F (35.7° C)c. respiratory rate of 20 breaths/minute

5. Which phrase best defines severe sepsis?a. sepsis-induced hypotension that persists despite adequate

fluid resuscitationb. systemic manifestations of infection plus a documented

infectionc. sepsis with organ dysfunction, tissue hypoperfusion, or

sepsis-induced hypotension

6. The phase of acute respiratory distress syndrome associ-ated with decreased compliance and increased dead space isa. the acute exudative phase.b. the fibroproliferative phase.c. the resolution phase.

7. Disseminated intravascular coagulation is associated with a. depleted platelets and coagulation factors.b. deactivated coagulation cascade.c. decreased risk of bleeding.

8. A sign of sepsis-induced acute cardiovascular systemfailure isa. bradycardia.b. hypertension.c. elevated central venous pressure.

9. Which lab test result is consistent with a diagnosis ofsepsis?a. elevated blood urea nitrogen levelb. hypercalcemiac. hypobilirubinemia

10. Which blood test is used to assess tissue perfusion in apatient with sepsis?

a. serum lactate levelsb. serum electrolyte levelsc. complete blood cell count

11. Which method of oxygen therapy is best for a patientwith sepsis?a. aerosol mask at 40% oxygenb. high-flow oxygen mask at 24% oxygenc. non-rebreather mask at 100% oxygen

12. Antibiotic therapy for suspected sepsis should begina. before obtaining blood cultures.b. immediately after obtaining two separate blood cultures.c. after blood culture results and sensitivity tests have been

received.

13. Which is used for volume expansion during sepsis?a. vasopressinb. lactated Ringer’s solutionc. albumin 5%

14. In the presence of severe sepsis, septic shock isdiagnosed when the patient’s lactate level is a. less than 3 mmol/L.b. between 3 and 4 mmol/L.c. greater than 4 mmol/L.

15. Before the causative organism is found, patients withsevere sepsis should receivea. broad-spectrum antibiotic therapy. b. antibiotic therapy to treat methicillin-resistant Staphylococcus

aureus.c. medication to treat candidemia.

16. Which medication is the drug ofchoice to restore hemodynamic sta-bility? a. norepinephrineb. dopaminec. vasopressin

17. Which patient with severe sepsisshouldn’t receive drotrecogin alfa?a. a hypotensive patientb. a patient with acute organ

dysfunctionc. a patient with gastrointestinal

bleeding

18. It’s recommended that a pa-tient with sepsis should have hisblood glucose level checkedeverya. 4 to 6 hours.b. 2 to 3 hours.c. 30 minutes to 1 hour.

Recognizing the signposts for sepsisGENERAL PURPOSE: To provide the professional nurse with an overview of how to recognize and care for a sepsis patient. LEARNINGOBJECTIVES: After reading this article and taking this test, you should be able to: 1. Describe the pathophysiology, signs and symptoms,complications, and lab tests associated with sepsis. 2. Identify the recommended medical and nursing interventions for managing sepsis.

2.5 ANCC CONTACT HOURS

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Recognizing the signposts for sepsis (page 40)B. Test Answers: Darken one circle for your answer to each question.

a b c1. m m m2. m m m3. m m m4. m m m


a b c9. m m m

10. m m m11. m m m12. m m m


a b c17. m m m18. m m m



a b c9. m m m

10. m m m11. m m m12. m m m


a b c17. m m m18. m m m19. m m m

C. Course Evaluation*

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Managing heart failure (page 12)B. Test Answers: Darken one circle for your answer to each question.

C. Course Evaluation*

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2. Was the journal home study format an effective way to present the material? q Yes q No

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and take the test ______?

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Registration deadline:

June 30, 2011

Contact hours: 2.5

Fee: $24.95

Test code: NMIE0509B

Registration deadline:

June 30, 2011

Contact hours: 2.5

Fee: $24.95

Test code: NMIE0509A

Mail completed test with registration fee to: Lippincott Williams & Wilkins,CE Group, 2710 Yorktowne Blvd., Brick, NJ 08723.

sepsis

Documents

complex cascade sepsis

local response

sepsis cases

incidence of sepsis

systemic inammatory

bodys response

acute phase response

number of older patients