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Recognizing the signposts for

sepsis
Sepsis is the number one Today is the fourth admission in a month
cause of death in the ICU, the for Mr. Hammill, 70, who has a recent med-
2.5 ical history of coronary artery bypass graft
surgery and atrial fibrillation and also a
ANCC 10th leading cause of death
history of coronary artery disease, chronic
CONTACT HOURS
worldwide, and the 11th leading
cause of death in the United obstructive pulmonary disease, diabetes,
gastroesophageal reflux disease, anemia,
and anxiety. Well known to you as an inter-
States. Older patients with
chronic illnesses are at high active and communicative man, you find
risk for developing this condi- that during this admission he’s irritable and
less talkative. You also note that he has gen-
eralized edema, coarse rhonchi in the ante-
tion. We discuss what you need
to know about sepsis and your rior lobes, and crackles in the bases of both
role in caring for a patient who lungs, and he’s coughing up tan-colored
sputum. This morning, he’s confused upon
awakening, and throughout the course of
has it.
the day you need to reorient him to his sur-
roundings.
By Margaret J. McCormick, RN, MS

His ability to answer questions correctly


Clinical Assistant Professor
Towson University • Towson, Md.
earlier in your shift suddenly declines. He’s
tachypneic with a respiratory rate of 32
The author has disclosed that she has no significant relationships
with or financial interest in any commercial companies that pertain

breaths/minute, an irregular pulse, and a


to this educational activity.

heart rate of 110 beats/minute. His serum


lactate level is 12 mmol/L. What’s going on
with Mr. Hammill? The healthcare team sus-

40 Nursing made Incredibly Easy! May/June 2009


May/June 2009 Nursing made Incredibly Easy! 41
pects sepsis on the basis of his age and clini-
cal findings.
A complex cascade
To start, let’s review what sepsis is and
If I break how it evolves.
through your
Sepsis = serious
A systemic inflammatory response to the
patient’s
presence of infection (such as Gram-positive
defenses, Endothelium

or Gram-negative bacteria, fungi, viruses,


sepsis may
result. mycobacteria, or parasites) that can
progress 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 to
diagnose clinically in this age group.
Babies and immunocompromised
Tissue factor

patients are also at increased risk.


The incidence of sepsis is reported as
three cases per 1,000 people; in hos-
pitalized patients, the incidence is 2%.
The rise in sepsis cases is believed to be
related to the growing number of im-
munocompromised patients, a greater
Monocyte

number of invasive procedures being


performed in the ICU, an increased number
of resistant organisms, and a rise in the
Inhibition

number of older patients with critical ill-


nesses.
What are the events that can lead to sep-
Activated

sis? Let’s find out.


protein C

A complex cascade Pathogens and


Inflammation is the body’s response to in-
endotoxin Inhibition

sults that arise from chemical, traumatic, or


infectious stimuli. The inflammatory cascade
Tissue factor

is a complex process that involves humoral


and cellular responses and complement and
cytokine cascades (see A complex cascade).
What does this mean? Following an insult to
the body, local cytokines are produced and
released into the circulation to promote a lo-
cal response. Growth factor stimulation and
recruitment of macrophages and platelets
Inflammatory

occur. The goal is homeostasis; however, if


response to infection

homeostasis doesn’t occur from the local re-


sponse to inflammation, the result is a sys-

42 Nursing made Incredibly Easy! May/June 2009


Activated
protein C

Coagulation cascade
Activated
protein C Plasminogen
activator
inhibitor-1

Factor VIIIa
Inactivation
Inactivation
Prevents
Proinflammatory activation
Factor Va
cytokines:
Inactivation
Interleukin-6

Interleukin-1
Thrombin Thrombin-activatable
fibrinolysis inhibitor
Tumor necrosis
factor-alpha

Fibrin
Neutrophil Fibrin clot

Interleukin-1 Limits Activated


Tumor necrosis adhesion protein C
factor-alpha

Thrombotic response Fibrinolytic response


to infection to infection

May/June 2009 Nursing made Incredibly Easy! 43


Here’s a handy
cheat sheet
with definitions
galore.

temic inflammatory reaction. liver increases fibrinogen and C-reactive


The most prominent systemic manifesta- protein production. Skeletal muscle catabo-
tion of inflammation is known as the acute lism provides amino acids that can be used
phase response. This constellation of sys- in the repair of tissue. IL-8 may perpetuate
temic effects usually begins within hours tissue inflammation. IL-6 and IL-10 aug-
or days of the onset of inflammation. ment the acute phase response by generat-
The release of cytokines, such as inter- ing additional proinflammatory mediators.
leukin (IL)-1, IL-6, and tumor necrosis The unregulated release of proinflamma-
factor (TNF), causes the thermoregula- tory mediators or cytokines can elicit toxic
tory center in the hypothalamus to reactions and promote endothelial cell-
produce an elevation in the leukocyte adhesion, releasing cell-damaging
patient’s body temperature, proteases and prostaglandins, which partici-
resulting in a fever. During the pate in the generation of fever, tachycardia,
acute phase response, the ventilation/perfusion abnormalities, and lac-
bone marrow produces more tic acidosis, and activating the clotting cas-
immature neutrophils and the cade. Endotoxins cause tissue damage by
releasing prostaglandins, and the resulting
cheat vasodilation and increased capillary perme-
ability allow fluid to enter the interstitial
Important definitions
space, causing edema and hypotension. The
Bacteremia: the presence of bacteria in the blood.
sheet

lack of oxygen at the cellular level causes the


Infection: the presence of microorganisms that trigger an inflam-

respiratory system to fail, followed by renal,


matory response.

gastrointestinal (GI), and liver failure.


Hypotension: a systolic BP of less than 90 mm Hg or a drop in

Platelet aggregation and thrombi form


systolic BP of greater than 40 mm Hg from the patient’s baseline

because of the increased viscosity of the


BP.

blood. This can result in decreased tissue


Sepsis: a systemic response to infection; may occur after a burn,
surgery, or serious illness and is manifested by two or more clinical
signs and symptoms: perfusion and the development of dissemi-
• temperature greater than 100.4° F (38° C) or less than 96.8° F (36° C)
nated intravascular coagulation (DIC), or
idiosyncratic bleeding and clotting. This can
• heart rate of greater than 90 beats/minute

ultimately lead to multiple organ damage


• respiratory rate of greater than 20 breaths/minute

and dysfunction.
• 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)
Pinning down the culprit
Sepsis can occur in people of all ages, but it’s
• hyperglycemia and abnormal clotting and bleeding.

more prevalent in older patients. In one na-


Severe sepsis: the presence of signs and symptoms of sepsis-related

tionwide study, it was found that patients


organ dysfunction, hypotension, or hypoperfusion; clinical signs and

older than age 65 accounted for 64.9% of all


symptoms include those of sepsis as well as:
• lactic acidosis
• oliguria sepsis cases. A possible reason for this high
• thrombocytopenia
incidence is the fact that older patients are
more likely to have Gram-negative infec-
• altered level of consciousness.

tions, particularly associated with pneumo-


Septic shock: shock associated with sepsis; characterized by symptoms

nia, and comorbid conditions. Possible


of sepsis plus hypotension and hypoperfusion despite adequate fluid vol-

causes of sepsis include:


ume replacement.

• pneumonia
SIRS: a syndrome resulting from a severe clinical insult that initiates an

• urinary tract infection (UTI)


overwhelming inflammatory response by the body.

• diarrhea or distension
MODS: the presence of altered function of one or more organs in an

• meningitis
acutely ill patient requiring intervention and support of the organs to

• cellulitis
achieve physiologic functioning required for homeostasis.

44 Nursing made Incredibly Easy! May/June 2009


• septic arthritis
• wound infection
Signs of acute organ
• endocarditis system failure
• catheter-related infection.
Sepsis may start with systemic inflamma-
Cardiovascular

tory response syndrome (SIRS). The diagno-


• Tachycardia

sis of SIRS requires two or more of the fol-


• Arrhythmias

lowing clinical findings:


• Hypotension

• body temperature of greater than 100.4° F


• Elevated central venous and pulmonary
artery pressures
(38° C) or less than 96.8° F (36° C)
• heart rate of greater than 90 beats/minute
Respiratory

• respiratory rate of greater than 20


• Tachypnea

breaths/minute or a partial pressure of car-


• Hypoxemia

bon dioxide measurement of less than 32


Renal

mm Hg
• Oliguria

• white blood cell (WBC) count of greater


• Anuria

than 12,000/mm3 or less than 4,000/mm3 or


• Elevated creatinine

greater than 10% immature forms of neu-


Hematologic

trophils or bands.
• Jaundice

A patient with systemic manifestations of


• Elevated liver enzymes

infection plus a documented infection has


• Decreased albumin

sepsis. A patient with sepsis complicated by


• Coagulopathy

organ dysfunction, tissue hypoperfusion (an


GI

elevated serum lactate level or oliguria), or


• Ileus (absent bowel sounds)

sepsis-induced hypotension (a systolic BP of


Hepatic

less than 90 mm Hg or a mean arterial pres-


• Thrombocytopenia

sure [MAP] of less than 70 mm Hg, or a


• Coagulopathy

decrease in systolic BP of greater than 40 mm


• Decreased protein C levels

Hg below normal for the patient’s age in the


• Increased D-dimer levels

absence of other causes) has severe sepsis. A


Neurologic

patient with sepsis-induced hypotension


• Altered consciousness

that persists despite adequate fluid resuscita-


• Confusion

tion and isn’t explained by other causes has


• Psychosis

septic shock.
cardia are seen during the first 12 to 24
Complication station hours, followed by a dramatic increase in
Complications associated with sepsis in- the work of breathing. The three phases of
clude acute respiratory distress syndrome ARDS are the acute exudative phase, which
(ARDS), acute renal failure, GI complica- is characterized by profound hypoxemia and
tions, DIC, and multiple organ dysfunction associated with inflammation and diffuse
syndrome (MODS). Let’s take a closer look. alveolar damage; the fibroproliferative
ARDS is defined as the abrupt onset of phase, which is associated with decreased
respiratory distress accompanied by three compliance and increased dead space; and
components: severe hypoxemia, bilateral the resolution phase, which may take 6 to 12
pulmonary infiltrates seen on X-ray, and the months or longer to resolve.
absence of heart failure or fluid overload. Acute renal failure may develop as a
Hypoxemia may be present before the onset result of endotoxins, which are powerful
of other clinical signs. Tachypnea and tachy- vasoconstrictors that can cause intravascular

May/June 2009 Nursing made Incredibly Easy! 45


Common medications used to treat sepsis
Classification 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 response


solution

Colloids
Albumin 5% Used for volume expansion May exacerbate renal insufficiency

Antibiotics
Cefotamine Used for Gram-negative coverage against Adjust dose in severe renal failure
Escherichia 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/minute
mirabilis, 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 levels
activity 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 output
smooth muscle contraction throughout the
vascular bed of the renal tubular epithelium

46 Nursing made Incredibly Easy! May/June 2009


clotting. The degree of renal damage is rela- patients with septic shock. Platelets are acute
tive to the severity and duration of the phase reactants and usually rise at the onset
shock. Acute tubular necrosis may occur of any serious stress. The platelet count will
because of severe ischemia to the kidneys. fall with persistent sepsis. An elevated WBC
With careful monitoring of urine output and count may predict bacterial infection. The
serum creatinine and blood urea nitrogen patient may have leukocytosis, leukopenia,
levels, acute renal failure is reversible. azotemia (an accumulation of nitrogenous
GI complications can develop when waste products in the blood), thrombocy-
there’s a redistribution of blood flow to the topenia, anemia, or hypoxemia.
mucosal layer of the GI tract. Superficial • coagulation studies. Assess prothrombin
lesions can cause stress ulcers in the stom- time (PT) and partial thromboplastin time.
ach. Bleeding is a common symptom, and Patients with sepsis often have a prolonged
hemorrhage can occur 2 to 10 days after the PT time. Patients with clinical evidence of
insult. coagulopathy require additional tests to
DIC is caused by activation of the coagula- detect the presence of DIC.
tion cascade, resulting in the formation of • arterial blood gas (ABG) analysis.
Septic shock
fibrin clots and thrombotic occlusion of small Measure serum lactate levels to assess tissue
can damage
and midsized vessels. The delayed removal perfusion. An elevated serum lactate level
all of us?
of fibrin occurs because of impaired fibrinol- (above 4 mmol/L) indicates significant tissue
Yikes!
ysis. Depletion of platelets and coagulation hypoperfusion and a shift from aerobic to
factors increase the risk of bleeding. Fibrin anaerobic metabolism. In severe cases, the
deposits in organs can cause ischemic dam- patient may have lactic acidosis.
age and organ failure. • cultures of sputum, urine, cerebrospinal
MODS occurs when multiple organs, such fluid, wound drainage, or respiratory secre-
as the kidneys, liver, lungs, brain, and heart, tions. Tissue Gram staining from the site of
are damaged as a consequence of septic the possible infection can provide guidance
shock. The mortality rate increases with the in the choice of antibiotic therapy. A spu-
number of failing organs. See Signs of acute tum culture can determine the presence of
organ system failure for more information. pneumonia; a urine culture can determine
the presence of UTI.
Lab tests at the ready How’s sepsis treated? That’s up next.
Early detection of sepsis is critical so that
appropriate intervention can be imple- Bundle up
mented. Aggressive treatment protocols According to the Surviving Sepsis Cam-
have been shown to decrease mortality paign’s guidelines for the management of
rates by 30% for severely septic patients and severe sepsis and septic shock, using a sep-
by 50% for patients who haven’t yet devel- sis bundle can reduce mortality in severe
oped the disease. cases. A bundle is defined as a group of in-
Lab tests to diagnose sepsis include: terventions related to a disease process that,
• metabolic studies, including evaluation of when implemented together, result in better
serum electrolyte levels. Often patients with outcomes than when implemented individ-
sepsis have hypocalcemia, hyper- or hypo- ually. Treatment for sepsis includes the fol-
glycemia, an elevated blood urea nitrogen lowing six interventions:
level, and mild hyperbilirubinemia. • give 100% oxygen via non-rebreather
• complete blood cell (CBC) count with dif- mask. Because the metabolic demands for
ferential and platelet count. An adequate oxygen are massively increased in sepsis,
hemoglobin level (7 to 9 g/dL for adults) is the need for intubation and mechanical ven-
necessary to ensure oxygen delivery in tilation may be required if ABG levels dete-

May/June 2009 Nursing made Incredibly Easy! 47


riorate and blood pH decreases. temic vascular resistance at 800 to 1,200
• obtain two separate blood cultures before dynes/sec/cm-5 The typical amount of
antibiotic therapy is initiated. At least two crystalloid solution for both severe sepsis
blood cultures should be drawn before an- and septic shock ranges from 4 to 8 liters.
tibiotic therapy initiation, with at least one Fluid challenges with 300 to 500 mL of crys-
drawn percutaneously and one drawn talloids or colloids may be given based on
through each vascular access device, unless BP and urine output. This extra fluid will
Antibiotics are the device was recently inserted (less than help blood flow to the organs. Careful mon-
imperative for 48 hours). Source control is also an impor- itoring is necessary to prevent overload in a
the patient tant strategy for certain types of sepsis pa- patient with known heart failure.
with sepsis. tients. Recent studies done on patients with • measure the patient’s lactate and hemo-
sepsis show that removing any infected de- globin-A lactate levels. Septic shock is diag-
vice and debriding necrotic or infectious tis- nosed when the lactate level is greater than
sue, especially in skin and soft tissue infec- 4 mmol/L in the presence of severe sepsis.
tions, are recommended. Drainage and A low hemoglobin value means that the
debridement may also be appropriate for amount of oxygen carried to the organs and
patients with empyema (the collection of tissue is reduced. If the hemoglobin level is
pus within an anatomic cavity), sinusitis, less than 7 g/dL, a blood transfusion
and infections of the chest and medi- should be considered.
astinum. • insert a urinary catheter to monitor
• initiate antibiotic therapy. Because sepsis hourly urine output. Urine output is a good
is caused by an infectious disease, one of indicator of how well the patient’s kidneys
the cornerstones of patient management is are being perfused. If the amount of urine
antibiotic therapy. The appropriateness and drained by the catheter is low, it could
timing of antibiotic coverage is important. mean that circulation to the body is im-
Initially, a broad-spectrum antibiotic should paired and fluid challenges are needed to
be used, with emphasis on the most likely restore perfusion.
pathogens, but should be discontinued Now let’s delve deeper into antibiotic
within 3 to 5 days. Antibiotic therapy is therapy and other medications used to treat
modified after cultures are available and an- sepsis (see Common medications used to treat
tibiotic susceptibility patterns are known. sepsis).
Single antibiotic therapy may last for 7 to 10
days and in certain cases may be longer, Meds up to bat
such as in patients with a slow response, According to the guidelines, antibiotic ther-
those who are immunologically deficient, apy should be started within the first hour,
or those with an area of infection that’s if possible. A recent study examined the
undrainable. Dosage adjustments may be timing of antibiotic therapy and found that
based on renal function. every additional hour without effective an-
• initiate fluid resuscitation. Another cor- tibiotic therapy can increase the risk of
nerstone of treatment is the infusion of I.V. death in patients with hypotensive sepsis
fluid to restore the circulating volume lost by 7.6% during the first 6 hours. The choice
as fluid leaks from capillaries. Crystalloid of antibiotic prescribed by the healthcare
solutions, such as 0.9% sodium chloride or provider depends on complex issues related
lactated Ringer’s solution, or colloids, such to the patient’s history, drug intolerances,
as albumin, will help to keep the MAP underlying diseases, clinical syndromes,
above 65 mm Hg. Wedge pressure should and susceptibility patterns of pathogens in
be maintained at 6 to 12 mm Hg; central ve- the community and hospital. Clinicians
nous pressure, 8 to 12 mm Hg; and sys- should be cognizant of the virulence and

48 Nursing made Incredibly Easy! May/June 2009


growing prevalence of methicillin-resistant microvasculature circulation associated with
Staphylococcus aureus infection and the pos- multiorgan dysfunction and death. Trials
sibility of candidemia when choosing ap- show that the use of drotrecogin alfa reduces I’m always
propriate antibiotic therapy. It’s recom- the risk of death among patients with severe looking for a
mended that patients with severe sepsis sepsis by 20% because it inhibits thrombosis way in...
receive broad-spectrum antibiotic therapy and inflammation and promotes fibrinolysis.
until the causative organism and antibiotic It also prevents microvascular dysfunction
susceptibilities are found. Although appro- and coagulation, improves tissue perfusion
priate cultures need to be obtained before and oxygenation, and reverses hypotension.
starting antibiotics, it shouldn’t delay ther- Drotrecogin alfa is recommended for
apy. Premixed antibiotics or bolus antibi- patients with severe sepsis or septic shock
otics may facilitate prompt administration. who are at high risk for death. Patients con-
Vasopressors, such as dopamine and nor- sidered for treatment should be carefully
epinephrine, are used to restore tissue perfu- evaluated. Due to its antithrombolytic effect,
sion pressure. Dopamine increases myocar- this drug is contraindicated if the patient is
dial contractility and is more likely to experiencing active internal bleeding; has
increase cardiac output; however, it may had recent head trauma, GI bleed-
increase the patient’s heart rate and produce ing, or surgery; or has an
tachyarrhythmias. Norepinephrine is a more epidural catheter in place. And
potent vasoconstrictor and has been found to it shouldn’t be given 2 hours
be more effective than dopamine in restoring before an invasive or surgical
hemodynamic stability. It’s considered to procedure. Recently, the FDA
be a first-line choice of drug therapy for has issued a label warning
patients with sepsis. The use of vasopressin about administering drotrecogin
was recently studied in the Vasopressin and alfa to patients with single organ
Septic Shock Trial. During this study, it was dysfunction who have recently
found that patients requiring vasopressors undergone surgery or those who may
(norepinephrine or vasopressin) for at least 6 not be at high risk for death.
hours who had one dysfunctional organ sys-
tem had no difference in 28-day survival. The role of the nurse will be
The use of corticosteroids may be helpful played by…
to decrease complement activity, platelet What should you do when caring for a pa-
activation, TNF, and proinflammatory tient with sepsis?
cytokines. Guidelines state that the use of Nursing interventions include:
corticosteroids is indicated for adult patients • infection control measures. It’s critical
with septic shock when hypotension remains that you strictly follow infection control
poorly responsive to adequate fluid resusci- measures, including practicing proper hand
tation and vasopressors. hygiene as outlined by the CDC.
Drotrecogin alfa was approved for use by • assessment and monitoring. Assess and
the FDA in 2001 for the treatment of severe document the patient’s vital signs at least
sepsis. This recombinant form of human acti- every hour. Monitor body temperature,
vated protein C is the first of a new category respiratory rate, BP, MAP and central ve-
of medications that act on the body’s re- nous pressure, heart rate, urine output,
sponse to infection at the level of the blood and oxygen saturation values. Lab moni-
vessel. The inflammatory cascade that occurs toring of a patient’s blood glucose level is
during severe sepsis causes activation of the recommended every 30 to 60 minutes be-
coagulation system associated with impaired cause tight glycemic control (under 150
fibrinolysis. This can result in changes in the mg/dL) has been shown to improve out-

May/June 2009 Nursing made Incredibly Easy! 49


Early ID of
developing
comes. Frequently perform neurologic tion. Despite the administration of I.V. flu-
sepsis and
immediate checks to assess any change in mental sta- ids, he remains hypotensive. He’s started on
management tus. Monitor for coagulation abnormalities. vasopressors in an attempt to maintain a
are key. If the patient starts oozing or bleeding MAP of greater than 65 mm Hg. His urine
from three separate sites (such as the nose, output from the indwelling catheter drops to
a wound, and the I.V. site) or has petechiae 10 mL/hr. He’s given additional I.V. colloids
or cyanosis, he may be developing DIC. and a total of 200 mL of albumin. Later that
Also be alert for the presence of cold, mot- night, his condition begins to improve.
tled, or cyanotic extremities because a mi-
crovascular occlusion forms clots to distal Signposts ahead
tissues. Report these findings to the health- Sepsis is a significant cause of morbidity
care provider. and mortality in older patients. The diagno-
• proper documentation. Documentation sis of sepsis can be particularly difficult in
should include the following: the type of this age group, and a high index of suspi-
respiratory support and results of ABG cion is necessary for early identification and
analysis, the type and location of I.V. intervention. Deterioration in the clinical
access, and the time and amount of condition of an older patient may be subtle
I.V. crystalloids, colloids, antibiotics, and easily missed, so each encounter may
or vasopressors given. Report and provide clinical clues that can alert you to
document results of lab tests such as changes in physiologic status, which may
the CBC count; electrolyte, blood glu- be an early manifestation of sepsis. By un-
cose, and lactate levels; and coagulation derstanding the signposts for sepsis, you’ll
studies. be able to recognize and rapidly identify a
• communication with the patient’s patient developing this condition so that
family. Families of patients with sep- immediate and appropriate management
sis may feel helpless during this critical can be implemented. ■
time. They need frequent explanations of
interventions and procedures, as well as Learn more about it
compassionate care. Communication about Dellinger RP, Levy MM, Carlet JM, et al. Surviving Sepsis
end-of-life issues and life-sustaining mea-
Campaign: international guidelines for management of se-
vere sepsis and septic shock: 2008. Crit Care Med. 2008;36
sures ahead of time allows the family to un- (1):296-327.
derstand what’s happening to their loved Dombrovskiy V, Martin A, Suderram J, Paz H. Use of
drotrecogin alpha (activated) for severe sepsis in New
one and make informed choices and deci- Jersey acute care hospitals. Am J Health Syst Pharm.
sions. 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-
On the road to recovery
So what’s happening with our patient, Mr. potension before initiation of effective antimicrobial ther-
Hammill? apy is the critical determinant of survival in human septic
shock. Crit Care Med. 2006;34(6):1589-1596.
Mr. Hammill’s condition is medically Martin GS. SAFE, VASST, LIPOS Trial 3, CORTICUS and
complex and he’s critically ill. His WBC more: implications for the Surviving Sepsis Campaign
count is 25,000/mm3 and sputum cultures
guidelines. http://www.medscape.com/viewarticle/
555167.
identify the source of sepsis as pneumonia. Picard KM, O’Donoghue SC, Young-Kershaw DA, Russell
Mr. Hammill is placed on a broad-spectrum KJ. Development and implementation of a multidiscipli-
nary sepsis protocol. Crit Care Nurse. 2006;26(3):43-54.
antibiotic. Over the course of the day, he
Porth CM. Essentials of Pathophysiology: Concepts of Altered
becomes more confused and then obtunded. Health States. Philadelphia, PA: Lippincott Williams &
His oxygen saturation value falls to 85% and Wilkins; 2004:334-335.

he becomes acutely hypotensive. He’s resus- Porth CM. Pathophysiology: Concepts of Altered Health
States. 7th ed. Philadelphia, PA: Lippincott Williams &
citated and placed on mechanical ventila- Wilkins; 2006:387-401.

50 Nursing made Incredibly Easy! May/June 2009


Robson WP, Daniel R. The sepsis six: helping patients to http://www.emedicine.com/MED/topic3372.htm.
survive sepsis. Br J Nurs. 2008;17(1):16-21. Smeltzer SC, Bare BG, Hinkle JL, Cheever KH. Brunner
Sakr Y, Reinhart K, Vincent JL, et al. Does dopamine ad- and Suddarth’s Textbook of Medical-Surgical Nursing. 11th
ministration in shock influence outcome? Results of the ed. Philadelphia, PA: Lippincott Williams & Wilkins;
Sepsis Occurrence in Acutely Ill Patients (SOAP) study. 2007:373.
Crit Care Med. 2006;34(3):589-597. Strategies for Managing Multisystem Disorders. Philadelphia,
Sharma S, Eschun G. Multisystem organ failure of sepsis. PA: Lippincott Williams & Wilkins; 2005:326-329.

On the Web
These online resources may be helpful to your patients and their families: The more
• eMedicine Health: Sepsis (blood infection): http://www.emedicinehealth.com/sepsis_blood_
infection/article_em.htm
CE, the
• Mayo Clinic: Sepsis: http://www.mayoclinic.com/health/sepsis/DS01004 merrier!
• 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.

For more than 38 additional continuing education


articles related to infection, go to Nursingcenter.com/CE.

Earn CE credit online:


Go to http://www.nursingcenter.com/CE/nmie
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INSTRUCTIONS
Recognizing the signposts for sepsis
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• On the print form, record your answers in the test answer • We also offer CE accounts for hospitals and other health care facilities on nurs-
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tion has only one correct answer. You may make copies of
these forms. PROVIDER ACCREDITATION
• Complete the registration information and course evalua- Lippincott Williams & Wilkins, publisher of Nursing made Incredibly Easy!, will
tion. Mail the completed form and registration fee of award 2.5 contact hours for this continuing nursing education activity.
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hours and an answer key to review your results.There is no District of Columbia and Florida #FBN2454. LWW home study activities are
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• Registration deadline is June 30, 2011. Your certificate is valid in all states.

May/June 2009 Nursing made Incredibly Easy! 51


2.5
ANCC CONTACT HOURS

Recognizing the signposts for sepsis


GENERAL PURPOSE: To provide the professional nurse with an overview of how to recognize and care for a sepsis patient. LEARNING
OBJECTIVES: 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.

1. Which statement most accurately describes sepsis? a. serum lactate levels


a. It’s a severe infection complicated by tissue hypoperfusion. b. serum electrolyte levels
b. It’s a systemic inflammatory response to the presence of c. complete blood cell count
infection.
c. It’s an infection-induced hypotensive state that doesn’t re- 11. Which method of oxygen therapy is best for a patient
spond to fluid resuscitation. with sepsis?
a. aerosol mask at 40% oxygen
2. The inflammatory cascade involves all of the following b. high-flow oxygen mask at 24% oxygen
except c. non-rebreather mask at 100% oxygen
a. production and release of local cytokines into the circulation.
b. inhibition of macrophages and platelets. 12. Antibiotic therapy for suspected sepsis should begin
c. release of tumor necrosis factor. a. before obtaining blood cultures.
b. immediately after obtaining two separate blood cultures.
3. Multisystem failure (respiratory, renal, GI, and liver) in c. after blood culture results and sensitivity tests have been
shock is due to received.
a. lack of oxygen at the cellular level.
b. decreased capillary permeability. 13. Which is used for volume expansion during sepsis?
c. intravascular fluid overload. a. vasopressin
b. lactated Ringer’s solution
4. Which isn’t a clinical sign of systemic inflammatory c. albumin 5%
response syndrome?
a. white blood cell count of 3,800 mm3 14. In the presence of severe sepsis, septic shock is
b. temperature of 96.2° F (35.7° C) diagnosed when the patient’s lactate level is
c. respiratory rate of 20 breaths/minute a. less than 3 mmol/L.
b. between 3 and 4 mmol/L.
5. Which phrase best defines severe sepsis? c. greater than 4 mmol/L.
a. sepsis-induced hypotension that persists despite adequate
fluid resuscitation 15. Before the causative organism is found, patients with
b. systemic manifestations of infection plus a documented severe sepsis should receive
infection a. broad-spectrum antibiotic therapy.
c. sepsis with organ dysfunction, tissue hypoperfusion, or b. antibiotic therapy to treat methicillin-resistant Staphylococcus
sepsis-induced hypotension aureus.
c. medication to treat candidemia.
6. The phase of acute respiratory distress syndrome associ-
ated with decreased compliance and increased dead space is 16. Which medication is the drug of
a. the acute exudative phase. choice to restore hemodynamic sta-
b. the fibroproliferative phase. bility? Ready? Set?
c. the resolution phase. a. norepinephrine
b. dopamine
Ace this test.
7. Disseminated intravascular coagulation is associated with c. vasopressin
a. depleted platelets and coagulation factors.
b. deactivated coagulation cascade. 17. Which patient with severe sepsis
c. decreased risk of bleeding. shouldn’t receive drotrecogin alfa?
a. a hypotensive patient
8. A sign of sepsis-induced acute cardiovascular system b. a patient with acute organ
failure is dysfunction
a. bradycardia. c. a patient with gastrointestinal
b. hypertension. bleeding
c. elevated central venous pressure.
18. It’s recommended that a pa-
9. Which lab test result is consistent with a diagnosis of tient with sepsis should have his
sepsis? blood glucose level checked
a. elevated blood urea nitrogen level every
b. hypercalcemia a. 4 to 6 hours.
c. hypobilirubinemia b. 2 to 3 hours.
c. 30 minutes to 1 hour.
10. Which blood test is used to assess tissue perfusion in a
patient with sepsis?

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52 Nursing made Incredibly Easy! May/June 2009


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Managing heart failure (page 12)


B. Test Answers: Darken one circle for your answer to each question.
a b c a b c a b c a b c a b c Registration deadline:
1. ❍ ❍ ❍ 5. ❍ ❍ ❍ 9. ❍ ❍ ❍ 13. ❍ ❍ ❍ 17. ❍ ❍ ❍ June 30, 2011
2. ❍ ❍ ❍ 6. ❍ ❍ ❍ 10. ❍ ❍ ❍ 14. ❍ ❍ ❍ 18. ❍ ❍ ❍ Contact hours: 2.5
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4. ❍ ❍ ❍ 8. ❍ ❍ ❍ 12. ❍ ❍ ❍ 16. ❍ ❍ ❍ Test code: NMIE0509A
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1. Did this CE activity's learning objectives relate to its general purpose? ❑ Yes ❑ No 4. How long in minutes did it take you to read the article ______ , study the material ______ ,
2. Was the journal home study format an effective way to present the material? ❑ Yes ❑ No and take the test ______?
3. Was the content relevant to your nursing practice? ❑ Yes ❑ No 5. Suggestion for future topics
____________________________________________________________________________________

Recognizing the signposts for sepsis (page 40)


B. Test Answers: Darken one circle for your answer to each question.
a b c a b c a b c a b c a b c Registration deadline:
1. ❍ ❍ ❍ 5. ❍ ❍ ❍ 9. ❍ ❍ ❍ 13. ❍ ❍ ❍ 17. ❍ ❍ ❍ June 30, 2011
2. ❍ ❍ ❍ 6. ❍ ❍ ❍ 10. ❍ ❍ ❍ 14. ❍ ❍ ❍ 18. ❍ ❍ ❍ Contact hours: 2.5
3. ❍ ❍ ❍ 7. ❍ ❍ ❍ 11. ❍ ❍ ❍ 15. ❍ ❍ ❍ Fee: $24.95
4. ❍ ❍ ❍ 8. ❍ ❍ ❍ 12. ❍ ❍ ❍ 16. ❍ ❍ ❍
Test code: NMIE0509B
C. Course Evaluation*
1. Did this CE activity's learning objectives relate to its general purpose? ❑ Yes ❑ No 4. How long in minutes did it take you to read the article ______ , study the material ______ ,
2. Was the journal home study format an effective way to present the material? ❑ Yes ❑ No and take the test ______?
3. Was the content relevant to your nursing practice? ❑ Yes ❑ No 5. Suggestion for future topics
____________________________________________________________________________________

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May/June 2009 Nursing made Incredibly Easy! 53