Transcript Case Study: Sepsis - Jill Collins MSN Portfolio

Case Study:
Sepsis
Jill Collins, Dana Hogan, Louisa Golay,
Krystal Morris & Wanda Schumacher
December 16, 2010
History of Present Illness
• 30 y/o pt presents to ED with
increasing mental status changes
and abdominal pain X 24 hrs per
skilled nursing facility
– Nursing home staff reports pt had
unwitnessed fall last NOC
• Patient appears diaphoretic,
increased respiratory rate, thready
pulses, flushed skin, hot to touch
• Pt unable to verbalize pain rating;
FACES score of 7-8 given from
observed grimacing and moaning
MEDICAL/SOCIAL HISTORY
MEDICAL
SOCIAL
• Medical History
• Patient single without
children, previously lived
alone
• Family denies pt using
tobacco, alcohol, or
recreational drugs
• Family unable to report if
pt is currently sexually
active
• Patient appears to have
strong support system in
place
– HIV
– End Stage Liver Disease
• Liver cirrhosis
• Hepatic Encephalopathy
– SIADH
– Diabetes Mellitus Type 2
• Surgical History
– Upper Gastrointestinal
Endoscopy
– Adenoidectomy
Previous Admissions
• Admitted 6 months ago with hepatic
encephalopathy, acute kidney injury,
hyperkalemia, EKG changes
• Hepatic encephalopathy resolved
with lactulose treatments, kidney
function improved with short term
dialysis
• Patient was discharged after a 2
month hospitalization to a skilled
nursing facility for rehabilitation
Current Medications
DM/ENCEPHALOPATHY
• Lactulose: 20g PO
Q4hours
• Rifaxamin: 400mg TID
• Novolog: 2-14 U SQ
per sliding scale with
meals
HIV
• Lamivudine: 50 mg
PO daily
• Ritonavir: 100mg PO
daily
• Zidovudine: 300mg
PO daily
• Darunavir: 400mg PO
BID
• Truvada: 200/300
combination dose PO
daily
Initial Assessment
• Vital signs: BP 65/32, HR 125, Resp 28,
O2 sat 85% on RA, Temp 40C
• Pt appears agitated and unable to follow
basic instructions
• Nursing home staff reports prior to ED
arrival, pt was very lethargic and
experiencing generalized weakness
• Skin flushed pink warm
Physical Examination
• Neuro: Perrla, generalized weakness,
oriented x1 to person, unable to
answer questions appropriately
• Cardio/Respiratory: Normal ST,
hypotensive, weak pulses in all
extremities, shallow/rapid breathing,
lung sounds crackles bases bilaterally
• GI/GU: Abdomen firm/distended, pt
moans with RUQ palpation, BS absent,
foley placed prior to pt arrival – no
documentation of placement date;
decreased urine output (10cc/hr;
amber in color, cloudy with sediment)
DIAGNOSES
WORKING DIAGNOSES
•
Hepatic encephalopathy
secondary to ESLD
– Altered mental status changes
– Recent hospitalization for
same diagnosis
•
Septic shock secondary
to possible urosepsis
– Vital sign presentation (meets
3 of the 4 criteria for hospital
sepsis protocol)
– Febrile
– Unknown foley placement
date and appearance of urine
– Immune system compromised
due to HIV
ALTERNATIVE DIAGNOSES
• Bowel perforation and/or
bowel obstruction
• Abdominal appearance
with absent bowel sounds
• Pyelonephritis
• Urine appearance and
quantity
• Subdural hemorrhage
• Mental status changes
(confusion)
• Recent fall at nursing
home
• Generalized weakness
OTHER DIAGNOSES
• Pneumonia
• Febrile, respiratory status, and
recent hospitalization with d/c
to nursing facility
• Stroke
• Altered mental status changes,
generalized weakness, and
recent fall
• Abdominal Aortic Aneurysm
• Abdominal assessment & severe
hypotension
DIAGNOSIS CONT.
SEPSIS WORKING
DIAGNOSES
• Urosepsis
• Sepsis caused by
pneumocysitc
pneumonia
• Sepsis caused by
bowel perforation or
obstruction
• SIRS from pancreatitis
and ESLD
FINAL DIAGNOSIS
SEVERE
UROSEPSIS
UROSEPSIS
• Definition: Severe Sepsis
• Suspected or proven
infection, plus a systemic
inflammatory response
(e.g. fever, tachycardia,
tachypnea, elevated white
blood cell count, altered
mental state, and
hyperglycemia in the
absence of diabetes) with
organ dysfunction (e.g.
hypotension, hypoxemia,
oliguria, metabolic
acidosis,
thrombocytopenia, or
obtundation). (Porth, 628)
• Epidemiology
• Estimated that more that
750,000 cases of sepsis
occur each year in the US
ultimately leading to
approximately 225,000
deaths. (Porth, 628)
• Severe Sepsis is the
leading cause of death in
non-coronary ICU’s
(www.acponline.org)
• Sepsis has a mortality rate
of about 40% currently in
the US
(www.merckmanuals.com)
PATHOPHYSIOLOGY
• Etiology
• Most likely caused by bacterial
organism in the urine which most
likely developed as a result of a
chronic indwelling foley catheter.
Most cases of sepsis are caused by
hospital-acquired gram-negative
bacilli or gram positive cocci and
often occur in
immunocompromised patients and
those with chronic and debilitating
diseases
(www.merckmanuals.com)
PATHOPHYSIOLOGY CONT.
• Mechanisms of the disease
• Immunocompromised by HIV and
diabetes mellitus
• Chronic indwelling catheter is
source for bacterial collection
• Decreased food and fluid intake
secondary to altered mental status
from hepatic encephalopathy
• Possible alteration in electrolytes
secondary to medication for
hepatic encephalopathy (lactulose)
PATHOPHYSIOLOGY CONT.
•
Pathogenesis of disease
• Starts with inflammatory trigger (bacteria)
• Proinflammatory mediators are stimulated (tumor necrosis
factor and IL-1)
• Cytokines cause neutrophil-endothelial cell adhesion,
activate the clotting mechanism, and generate
microthrombi.
• Other mediators released including leukotrienes,
lipoxygenase, histamine, bradykinin, serotonin, and IL-2.
• These are opposed by anti-inflammatory mediators like IL-4
and IL-10 which results in a negative feedback mechanism.
• Vasoactive mediators cause blood flow to bypass capillary
exchange vessels.
• Poor capillary flow from the shunting along with capillary
obstruction by microthrombi decreases the delivery of
oxygen and impairs removal of carbon dioxide and waste
products.
• Decreased perfusion causes dysfunction and sometimes
failure of one or more organs, including the kidneys,lungs,
liver, brain, and heart.
• Coagulopathy can develop because of intravascular
coagulation with comsumption of major clotting factors.
(www.merckmanuals.com)
PATHOPHYSIOLOGY CONT.
•
Relation of pathology to history and clinical
manifestations
• Pt. immunocompromised by HIV, DM and cirrhosis
• Indwelling catheter source of bacterial growth and
proliferation
• Bacteria in urinary tract eventually trigged the
pathophysiologic process discussed in previous slide.
• Processes eventually lead to decreased perfusion to organs
which probably caused the altered mental status and
possibly the abdominal pain (also caused by the UTI)
• Hypotension occurs secondary to the vasodilation caused by
the inflammatory response. Tachycardia then ensues in an
attempt to keep blood pressure and cardiac output up.
Tachypnea is an attempt of the body to remove excess acid
buildup as well as the decreased availabilty of oxygen
(hypoxemia)caused by the sepsis process. Fever occurs as
a result of the energy expenditure needed to fight the
bacterial invasion.
SEPSIS TABLE
SIRS
Early
Sepsis
Sepsis
Severe Sepsis
Septic Shock
Infection
NO
Yes
Yes
Yes
Yes
Temp
>38.5 or < 35
>100.4 or <96.8
>38.5 or < 35
>100.4 or <96.8
Heart rate
>90
>90
>90
Resp rate
>20 or PaCO2<32
>20 or PaCO2<32
crackles* early sign
>20 crackles *early
sign!!!
>20
PaO2 < 72
PaO2 < 70
Normal or SBP 20-40
below baseline, pp
widened >40
pp widened >40
<90 or 40 below
baseline, pp
narrowed <40
Flushed pink warm,
edema
Flushed pink warm,
edema
Pale, cool, creeping
mottling
Hypoxemia
BP
Normal or SBP 20-40
below baseline, pp
widened >40
Skin color
Sub normal
>90
>90
WBC
>12,000, <4000 or
>10% immature
bands
UO
WNL or elevated WNL or elevated <30 ml/hr,
olguria
Altered LOC
Oliguria, anuria
Resp Alkalosis
Metabolic lactic
acidosis
LOC
Acid base
>12,000, <4000 or
>10% immature
bands
Resp alkalosis
initially
Elevated lactate
level
Confusion coma
DIAGNOSTIC TESTING
FOR SEPSIS
•
•
•
•
•
•
•
•
•
•
WBC with diff
Chemistry
Blood Cultures
Liver function
Cortisol
ABG
Lactic Acid
UA w/ C&S
CXR
Sputum C & S
FOR ALTERNATE DX
• Subdural hemorrhage
• CT of head
• Hepatic encephalopathy
secondary to ESLD
• Chemistry
• Liver functions
CBC with Differential
Lab
Normal
Client
Hemoglobin
14-18
8.8
Hematocrit
42-52
23.5
150-400
56
WBC
4.3-10
1.9
Neutrophils
55-70
76
Platelets
Bands
Lymphocytes
Monocytes
PTT
PT (INR)
8
20-40
13
2-8
3
20-45
67
<2
5
Complete Chemistry
Lab
Normal
Client
Sodium
136 - 145
125
Potassium
3.5 – 5.0
5.1
Chloride
98 – 106
99
CO2
23 – 30
15
Anion Gap
8 – 12
23
BUN
10 – 20
35
Creatinine
.6 – 1.2
2.5
Glucose
60-110
205
Albumin
3.5 - 5
2.0
Lactate
.5 - 2
7.28
Ammonia
15 - 45
96
Goal greater
than 70
51
Scvo2
ABG’s
Lab
PH
CO2
HCO3
PO2
Normal
7.35 - 7.45
35 -45
21 - 28
80 - 100
Client
7.25
55
24
83
Cortisol and Liver Functions
Lab
Normal
Client
Total Bilirubin
.3 – 1.0
30.8
AST
0 – 35
822
ALT
4 – 36
266
30 - 120
47
5 – 20
15.7
ALK Phos
Cortisol
Urinalysis
LAB
NORMAL
CLIENT
Color
Amber
Amber
Turbidity
Clear
1+
1.005 – 1.030
1.013
pH
4.6 – 8.0
6.5
Ketones
Negative
Negative
Protein
Negative
1+
Blood
Negative
Trace
Bilirubin
Negative
Positive
Leukocytes
Negative
Trace
WBC
0–4
2-10
RBC
0–2
2-10
Specific Gravity
Sediment
Few
Bacteria
Packed
WBC Clumps
Present
SURVIVING SEPSIS CAMPAIGN
NATIONAL GOALS: TREATMENT
• Immediately on arrival:
• STAT lactate, random cortisol, SCO2, PT/PTT,
fibrinogen, d-dimer, chemistry, CBC with Differential
• Blood, urine, and sputum cultures
• Prior to antibiotic administration if possible
• Cultures preferably from 2 peripheral sites,
cultures only from a line if line infection is a
concern
• Urine cultures should be obtained using clean
catch technique or from a foley catheter
SURVIVING SEPSIS CAMPAIGN
NATIONAL GOALS: TREATMENT
• Early Therapy
• Start in ED
• Focus on early
recognition and TX
• Studies show early,
appropriate TX (within
6 hrs of ED admission)
decreased 28 day
mortality rates by 16%
• Transfer to ICU
• Start with ABC’s
• Establish a patent
airway (patient
lethargic)
• Insure proper
oxygenation(sats were
85% on RA. ABG’s did
not improve on NRB so
patient was intubated
on placed on ventilator)
• Insure proper
circulation
SURVIVING SEPSIS: TREATMENT
WITHIN 1 HOUR
• Antibiotic Therapy
– Standard-Broad spectrum therapy
• Vancomycin 1000mg-1500mg IV Q 12 hours
• Levaquin 500-750mg IV Q12 hours
• Zosyn 2.25-4.5 mg IV Q 6 hours
• If patient is allergic to any of these antibiotics,
alternative medications can be used.
• Random Vancomycin trough levels need to be obtained
in order to appropriately dose this medication.
Vancomycin can cause impaired renal function
SURVIVING SEPSIS: WITHIN 6 HOURS
• Central Venous Pressure (CVP) goal 8-12
• Optimization through Normal Saline fluid boluses
• If less than 8, administer 500ml NS over 10
minutes
• Recheck CVP Q15 minutes and repeat 500ml
boluses until CVP is 8-12
• When goal is achieved, continue NS at 150ml/hr
• 250ml 5% Albumin can be used for a CVP less
than 4
• Lactate Monitoring
• Redraw lactates Q4 hours until less than 2
SURVIVING SEPSIS: WITHIN 6 HOURS
• Mean Arterial Pressure (MAP) goal 65
• MAP is often optimized through fluid resuscitation
with optimizing the CVP
• If MAP remains less than 65, give vasopressor of
choice:
• Levophed (norepinepherine)
• Begin with .01mcg/kg/min, titrate until MAP is
65 with a maximum dose of .3mcg/kg/min
• Vasopressin
• Consider at a set rate of 2.4 U/hr (standard)
• Can also be ordered as a titration with a range
of .6-3.6 U/hr
SURVIVING SEPSIS: WITHIN 6 HOURS
• ScV02 greater than 70
– Draw Q1 hour until optimized
– Continuous Scvo2 monitoring can be obtained with
the placement of a precept catheter
– To optimize Scvo2:
• If Hgb less than 10, transfuse 1 unit PRBCs, then
recheck level
• Consider dobutamine at 2.5mcg/kg/min if Hgb is
greater than 10
– Increase Q30 minutes until Scvo2 meets goal.
Do not exceed 20mcg/kg/min
SURVIVING SEPSIS: WITHIN 24 HOURS
• Evaluated and started on low dose steroids
• Hydrocortisone 100mg Q8 after reviewing cortisol
level on labs
• If level is greater than 25mcg/dL, do not give
steroids
• Glucose less than 150
• Insulin drip initiated if patient’s glucose is greater
than 150
• Keep in mind that steroid use and antibiotics
will often can an increase in blood glucose
levels
• Evaluate for need of Activated Protein C (Xigris)
Treatment
• Activated Protein C
(Xigris)
• Costly
• Decreased mortality
by 20%
• FDA approved
• Early administration
• Risk of increased
bleeding
• Steroids
• Antibiotics
• Remove sources of
infection
• Glycemic Control
• Active cooling
• Renal function
(consider CRRT if
needed)
Treatment
• WASH YOUR HANDS
• Strict aseptic/sterile
techniques
• Safety
• BSI
• Frequent position changes
• Inspect oral cavity QD
• Support/Educate Pt and
family
References

Porth C., Matfin G. (2009). Pathophysiology: Concepts of Altered Health States.
Philadelphia, PA. Lipppincott Williams & Wilkins.

Merck Manual Online. (2010). Retrieved December 4, 2010, from
http://www.merckmanuals.com

Harkins M.D., M. (n.d.). ACP Online. Retrieved December 4th, 2010, from
http://www.acponline.org/about_acp/chapters/nm/harkins/ppt


The University of Kansas Adult Severe Sepsis/Septic Shock Order Set
Dellinger, R. P., Levy, M. M., Carlet, J. M., Bion, J., Parker, M. M., Jaeschke,
R., Vincent, J. L. (2008). Surviving sepsis campaign: International guidelines
for management of severe sepsis and septic shock: 2008. Intensive Care
Medicine, 34, 17-60.

Institute for Healthcare Improvement. (2010). First steps and measures to reduce
sepsis mortality. Retrieved from
www.ihi.org/IHI/Topics/CriticalCare/Sepsis/ImprovementStories/FirstStepsan
dMeasures.org

Institute for Health Care Improvement. (2010). Sepsis. Retrieved from
www.ihi.org/Topics/Criticalcare/sepsis
THANK YOU!!!
QUESTIONS?????