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PROCALCITONIN: ADVANCING DECISION MAKING IN SEPSIS
Sean-Xavier Neath, M.D., Ph.D.Assistant Clinical Professor of MedicineDepartment of Emergency MedicineUniversity of California, San Diego
2
OBJECTIVES
• Explore the scope of sepsis, its costs and effects on the healthcare system
• Identify the difficulties associated with the rapid diagnosis of sepsis with a focus on the differentiation of bacterial from non-bacterial causes of SIRS
• Utilize the performance characteristics of the biomarker procalcitonin (PCT) as a marker of sepsis or significant bacterial infection
• Interpret PCT levels and understand current PCT utilization in the hospital
3
DISCLOSURES
1) Consultant relationships with biomedical companies working on biomarkers in acute disease states
Thermo Fisher ScientificBRAHMS
2) Employed by the University of California, San Diego Medical Center as an Assistant Professor of Clinical Medicine, Department of Emergency Medicine
4
WHAT IS SEPSIS?
• Whole Body Inflammatory State plus Infection
5
SYSTEMIC INFLAMMATORY RESPONSE SYNDROME (SIRS)
• Systemic inflammatory response to a variety of severe clinical insults. Manifested by two or more of the following:
• Temperature >38ºC or <36ºC• Heart rate >90 beats/min• Respiratory rate >20 breaths/min or PaCO2 <32 mm Hg• WBC >12,000/mm3, <4000/mm3, or >10% immature (band)
forms
ACCP/SCCM Consensus Statement. Chest. 1992;101:1644-1655.
6Slide
SEPSIS: ACCP/SCCM DEFINITIONS
• Sepsis• Systemic response to infection – i.e., confirmed or suspected
infection plus 2 SIRS criteria• Severe Sepsis
• Sepsis associated with organ dysfunction, hypoperfusion, or hypotension
• Septic Shock• Severe Sepsis that cannot be resuscitated or stabilized with IV fluids
alone
ACCP/SCCM Consensus Statement. Chest. 1992;101:1644.
InfectionInfection
ParasiteParasite
VirusVirus
FungusFungus
BacteriaBacteriaTraumaTrauma
BurnsBurns
SepsisSepsis SIRSSIRSSevereSevereSepsisSepsis
SevereSevereSIRSSIRS
Adapted from SCCM ACCP Consensus Guidelines
shock
BSIBSI
8
Martin GS et al. NEJM 2003;348:1346
POPULATION ADJUSTED INCIDENCE OF SEPSIS (USA)
9
Martin GS et al. NEJM 2003;348:1346
CASES OF SEPSIS BY PATHOGEN (USA)
10
INFECTION SOURCE IN SEVERE SEPSIS
44.0%
17.3%9.1%
8.6%
6.6%
2.2%
8.0%
6.0%
10.8%Respiratory
Bacteremia
GU
Abdomen
Soft tissue
Device
CNS
Endocarditis
Other
Angus DC et al. Crit Care Med. 2001; 29:1303
11
DETERMINANTS OF MORTALITY
• Source control is most vital factor• Resuscitation/re-establish perfusion in 6 hrs• Appropriate antibiotic therapy within 1 hr of hypotension
12
TREATMENT OF SEPTIC SHOCK
• Source Control When Possible• Based on Early Goal Directed Therapy• Broad, high dose, rapid administration of antibiotics• Consider Activated Protein C• Minimal role for steroids
Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock, 2008. Critical Care Med
13
• Differentiation between sepsis and non-infectious causes of SIRS is complicated
• The large number of patients presenting to the ER at the same time can limit the ability to obtain comprehensive histories and physical examinations
DIFFICULTIES IN DIAGNOSIS AND TREATING SEPSIS IN THE EMERGENCY DEPARTMENT
14
• Scoring systems and commonly available diagnostic tools provide limited value in determining which patients will have a poor outcome
• Initial vital signs can be incomplete, an accurate core temperature can be lacking
• These limitations often result in the delayed diagnosis of sepsis which in turn delays treatment, increases hospital length-of-stay, increases costs and leads to increased preventable mortality
DIFFICULTIES IN DIAGNOSIS AND TREATING SEPSIS IN THE EMERGENCY DEPARTMENT
15 Kumar A. et al., Crit Care Med 2006, 34:1286
DURATION OF HYPOTENSION BEFORE INITIATION OF EFFECTIVE ANTIMICROBIAL THERAPY IS THE CRITICAL DETERMINANT OF SURVIVAL IN HUMAN SEPTIC SHOCK
16
FAILURE TO INTERVENE QUICKLY CAN BE FATAL
Sebat CCM 2007; 35: 2568
17
• Initial Resuscitation• Diagnosis• Antibiotic therapy• Source Control• Fluid therapy• Vasopressors• Inotropic Therapy• Steroids• Recombinant Human Activate
d Protein C (rhAPC) [drotrecogin alfa (activated)]
Blood Product Administration
Mechanical Ventilation
Sedation, Analgesia, and Neuromuscular Blockade in Sepsis
Glucose Control
Renal Replacement
Bicarbonate Therapy
Deep Vein Thrombosis Prophylaxis
Stress Ulcer Prophylaxis
Limitation of Support
Key Areas of Sepsis Management
Dellinger, et. al. Crit Care Med 2004, 32: 858-873.
ROLE OF PROCALCITONIN IN INITIAL SEPSIS MANAGEMENT
19
WHY PROCALCITONIN?
Integrated use of PCT with other clinical and laboratory informationpermits:•Increased accuracy of clinical diagnosis of relevant bacterial infection / sepsis
•Improved clinical decision making and patient management
20
• Simple blood test specific for bacterial infection• During severe bacterial infections and sepsis, blood levels rise rapidly (up to x100K) – no
elevation from viral infections• Is the Standard of Care for much of Europe in the management of infection and sepsis
PROCALCITONIN – A BIOMARKER FOR THE ASSESSMENT OF CRITICALLY ILL PATIENTS AT RISK FOR SEVERE BACTERIAL INFECTION AND SEPSIS
Morgenthaler N. et al., Clin Lab 2002, 48: 263-270
21
PROCALCITONIN – NORMALLY AN INTERMEDIATE PRODUCT IN THE SYNTHESIS OF CALCITONIN
N-Pro Calcitonin Katacalcin
N C
1 57 60 91 96 116
After P. Linscheid, Endocrinology 2003
LOW PCT values in the blood of healthy persons: 46.7 pg/ml (97.5 percentile); median = 12.7 pg/ml*
Morgenthaler N. et al., Clin Lab 2002, 48: 263-270
Thyroid
22
Alternative synthesis of PCT• Bacterial toxins (gram+/-) and cytokines stimulate production of PCT in all
parenchymal tissues• PCT is immediately released into bloodstream• This process can be blocked during viral infections
PROCALCITONIN – PRESENCE OF BACTERIAL INFECTION STIMULATES PCT PRODUCTION
Adapted from Christ-Crain et al. 2005
23
Calcitonin: Sources ofproduction in healthy
people
Müller B. et al., JCEM 2001
• In bacterial infection, PCT is produced and released into circulation from the entire body
HIGHLY SPECIFIC INDUCTION AND RELEASE OF PCT DUE TO BACTERIAL INFECTION
Healthy Sepsis
PCT:Sources of Productionin Septic Patients
24
• In critically ill patients, PCT levels elevate in correlation to the severity of bacterial infection
• In healthy people, PCT concentration are found below 0.05ng/ml• Concentrations exceeding 0.5ng/ml can be interpreted as abnormal
PCT LEVEL INCREASE = INCREASED SIGNIFICANCE OF BACTERIAL INFECTION
Healthy Individuals
Local Infections
Systemic Infections (Sepsis)
Severe Sepsis
Septic Shock
0.05 ng/ml
0.5 ng/ml
2 ng/ml
25
• IFN- released in viral infection, blocks the activation of PCT production, therefore in viral infection PCT levelsremain normally low
HIGHLY SPECIFIC INDUCTION AND RELEASE OF PCT DUE TO BACTERIAL INFECTION
Adapted from Christ-Crain et al. 2005
26
Easy to measure, not invasive, relatively inexpensiveBiomarker Testing (PCT)
Slow kinetics , high impact of inflammation (specificity), suppressed by corticosteroids, relatively inexpensive
BENEFITS AND LIMITATIONS OF OTHER SEPSIS DIAGNOSTIC TOOLS
Microbiology (Blood Culture)
Imaging (X-Ray, Hr-CT)
Molecular Biological Testing
Biopsy
C-Reactive Protein (CRP)
Standard of care, time to result, ?Sens., ? Spec.
Availability, costs, variability of source detection
Invasive, relatively expensive
Availability, costs, time to results
27Simon L. et al. Clin Infect Dis. 2004; 39:206-217.
• PCT levels accurately differentiate sepsis from noninfectious inflammation*• PCT has been demonstrated to be the best marker for differentiating patients with sepsis from
those with systemic inflammatory reaction not related to infectious cause
DIAGNOSTIC ACCURACY OF PCT COMPARED TO OTHER BIOMARKERS USED IN SEPSIS
Sensitivity: 89%Specificity: 94%
NPV: 90% / PPV: 94%
28Harbarth S et.al. AM J Resp Crit Care Med. 2001; 164:396-402
• When PCT is used as a reference, the sensitivity and specificity of sepsis diagnosis can be significantly increased compared with conventional clinical parameters.
ADDING PCT RESULTS TO CLINICAL ASSESSMENT IMPROVES THE ACCURACY OF THE EARLY CLINICAL DIAGNOSIS OF SEPSIS
AUC with PCT: 0.94AUC without PCT: 0.74
29
• PCT can aid in the diagnosis and severity stratification in patients suspected of sepsis, severe sepsis, and septic shock.
• In multiple studies, PCT has demonstrated a high sensitivity and specificity for the differentiation of sepsis from SIRS (Systemic Inflammatory Response Syndrome)
• PCT levels can be useful for the management of patients after surgery or transplant and in peritonitis
PCT LEVELS INCREASE ACCORDING TO SEVERITY OF SEPSIS
Harbarth S et al. Am J Respir Crit Care Med 2001, 164: 396-402 ; Meisner M et al., Critical Care 1999, 3(1): 45-50 ; Krüger S. et al., Eur Respir J 2008; 31: 349–355
30
• PCT used in early detection of infection after liver transplantation – differentiation from rejection
ADDING PCT RESULTS TO CLINICAL ASSESSMENT IMPROVES THE ACCURACY OF THE EARLY CLINICAL DIAGNOSIS OF INFECTION POST ORGAN TRANSPLANT
PCT plasma concentrations in 16 patients without postoperative complications after Liver-Transplantation, Tx: day of transplantation.
PCT plasma concentrations in infection and rejection (n = 11), day 0: day of diagnosis
Kuse ER et al., Crit Care Med 2000; 28: 555-559
31
• Clinical symptoms alone are often insufficient for early and accurate diagnosis• PCT levels, can be observed within 3-6 hours after an infectious challenge with a
peak - up to 1000 ng/ml - after 6-12 hrs. Half-life: ~24hrs• Specific to bacterial origin of infection and reflects the severity of the infection
PCT KINETICS PROVIDE IMPORTANT INFORMATION ON PROGNOSIS OF SEPSIS PATIENTS
Brunkhorst FM et al., Intens. Care Med (1998) 24: 888-892
32
INTERPRETING PROCALCITONIN VALUES
33
• Newborn < 48hr - increased PCT values (physiological peak)• On 3rd day after birth, normal adult reference ranges apply
• Primary inflammation syndrome following trauma: multiple trauma, extensive burns, major surgery (cardiac, transplant, abdominal)• Rapid decrease (half-life 24hr) in the absence of bacterial infection
• Medullary C-cell cancers of the thyroid, pulmonary small-cell carcinoma and bronchial carcinoma
• Prolonged circulatory failure (e.g.. cardiogenic shock, hemorrhagic shock, thermal shock)
• Treatments that can cause a cytokine storm e.g. OKT3, anti-lymphocyte globulins, etc.
PCT RELEASE IN THE ABSENCE OF INFECTION
34
INFECTEDUNINFECTED
C Chiesa et al. CID 1997
• In early onset neonatal sepsis PCT provides a clear differentiation of infected from uninfected neonates in the first 2 days of life
• In neonates the PCT values are physiologically and in relation to their age increased.
• A peak is reached at 24 h with Median at 2 ng/ml and 95%-Percentile at 20 ng/ml.
• After 3 days the normal values for children and adults apply.
ADDING PCT RESULTS TO CLINICAL ASSESSMENT IMPROVES THE ACCURACY OF THE EARLY CLINICAL DIAGNOSIS OF SEPSIS IN NEONATES
Time (hours) Time (hours)
PCT (ng/ml)
PCT (ng/ml)
35
CONDITIONS OF BACTERIAL INFECTION WHERE PCT MAY BE LOW IN THE PRESENCE OF BACTERIAL INFECTION
Low PCT levels in the presence of bacterial infection may occur:
• Early course of infection: Re-measure in 6-12hrs• Subacute Endocarditis• Localized infections
36
• PCT values must always be interpreted within the clinical context of each individual patient
• Serial measurement is preferred to assess the situation in real-time
• Always pay attention to conditions that may influence the PCT level
• Always consider the dynamics of the disease process (which affect onset of PCT production)
INTERPRETATION OF PCT LEVELS
37
• Rapid kinetics: detectable 3 hours after infection has begun, with a peak after 6-12 hrs.
• Peak values up to 1000 ng/ml• Half-life: ~ to 24 hrs• Non or minor dependence on renal function
PCT KINETICS AFTER AN INFECTIOUS CHALLENGE
Brunkhorst FM et al., Intens. Care Med (1998) 24: 888-892
Brunkhorst FM et al., Intens. Care Med (1998) 24: 888-892
38
• Elevated / rising PCT levels• Systemic response to the infection - indicates that
infection is developing or is outside the control of the immune system
• Risk for further progression
• Low PCT levels despite clinical signs and symptoms• Self-limiting bacterial infection• Non-infectious cause• Early phase of infection
PCT REFLECTS THE RESPONSE OF THE ORGANISM TO THE BACTERIAL CHALLENGE
39
PROCALCITONIN UTILIZATION TO IMPROVE PATIENT CARE IN THE HOSPITAL
40
NO PCT INCREASE IN BACTERIAL CONTAMINATION, ONLY IN REAL BACTERIAL INFECTION
• In addition to clinical and microbiological parameters, PCT may help discriminate blood stream infections from blood culture contamination due to coagulase-negative staphylococci
• At a cut-off of 0.1ng/ml sensitivities and specificities were
• Day –1 of BC: 86% and 60%• Day 0 of BC: 100% and 86%
• CRP could discriminate only on day +1, but not as clear-cut as PCT
Schuetz P. et al., Infection 2007;35 (5): 352-5
41
• Current guidelines recommend blood culture sampling from hospitalized patients with suspected CAP. Is there a way to reduce the patient harm, costs and errors associated with these recommendations?
• Prospective cohort study with derivation and validation set including 925 patients with CAP who underwent blood culture sampling on hospital admission.
PCT LEVELS PREDICT BACTEREMIA IN PATIENTS WITH COMMUNITY ACQUIRE PNEUMONIA (CAP)
Muller et al. CHEST July 2010
42
PCT PREDICTS BACTEREMIA IN PATIENTS WITH CAP: PATIENT FLOW IN DERIVATION AND VALIDATION COHORTS
Muller et al. CHEST July 2010
43
PCT CUTOFF OF 0.1 ENABLES REDUCTION OF BLOOD CULTURES BY 12.6% AND IDENTIFIES 99% OF POSITIVE BLOOD CULTURES
Muller et al. CHEST July 2010
44
• PCT levels accurately predicted blood culture positivity in patients with CAP.
• PCT measurement demonstrated the potential to reduce the number of blood cultures drawn in the ED to better implement resources
• The use of PCT in targeting rational blood culture utilization allows for more directing allocation of limited health-care resources.
PCT LEVELS PREDICT BACTEREMIA IN PATIENTS WITH COMMUNITY ACQUIRE PNEUMONIA
Muller et al. CHEST July 2010
46
Mortality by PCT level
0%
2%
4%
6%
8%
10%
12%
0 5 10 15 20 25 30
Day
Mo
rtal
ity,
%
≥ 0.1
< 0.1
Huang, et.al., Annals of Emergency Medicine, Vol 51, March 2008
• PCT can be used for Risk stratification of patients with CAP• Low PCT levels identify patients presenting in the ED with Pneumonia that have a low
risk for mortality (N=1,651).
PCT RESULTS PROVIDE IMPORTANT INFORMATION ON PROGNOSIS OF CAP PATIENTS IN EMERGENCY ROOM
PCT
PCT
47
• Decreasing PCT levels in patients with sepsis indicate effective treatment of the underlying infection
• Persistently elevated PCT levels indicate a possible treatment failure• When integrated into the management of septic patients, PCT can help clinicians to
manage septic patients more efficiently
SERIAL MEASUREMENT OF PCT PROVIDES A CLEARER PICTURE OF THE PATIENT’S RESPONSE TO ANTIBIOTIC TREATMENT.
Stueber, F. University of Bonn, Lecture at ISICEM, Brussels 2001
48Nobre V. et alAM Resp Crit Care Med 2008: 177:498-505
• Effect of PCT-guided management in patients with sepsis on ICU length of stay
PCT GUIDANCE IN ANTIBIOTIC USAGE EFFECTS ON LENGTH OF STAY
49Nobre V. et alAM Resp Crit Care Med 2008: 177:498-505
• Effect of PCT-guided management in patients with sepsis on ICU length of stay
PCT GUIDANCE ON EFFECT ON LENGTH OF ICU STAY
50Nobre V. et al AM Resp Crit Care Med 2008: 177:498-505
KEY TAKEAWAY:
Tailoring of AB treatment using PCT to the individual patient needs safely led to a reduction of average treatment duration from 12 to 5 days with same outcome
PCT GUIDANCE IN ANTIBIOTIC USAGE HAS BEEN SHOWN TO SIGNIFICANTLY SHORTEN THE TIME PATIENTS NEED TO BE ON ANTIBIOTICS
51
EFFECT OF PCT TESTING ON ANTIBIOTIC USE – A MULTICENTER, RANDOMIZED CONTROL TRIAL
The ProHOSP Trial
• Lower respiratory tract infections (LRTI)• Most frequent indication for antibiotic prescriptions
in the Northwestern hemisphere• 75% of patients are treated with antibiotics• Predominantly viral origin of infection
• Procalcitonin (PCT) algorithm • Reduced antibiotic use in patients with LRTIs
51
Schuetz P et al. J Am Med Assoc. 2009;302:1059-66.
52
STUDY DESIGN
• Multicenter, noninferiority, randomized controlled trial
• Patients • Randomized to administration of antibiotics based on PCT algorithm• Cutoff ranges for initiating or stopping antibiotics (PCT group) or
standard guidelines (control) • Serum PCT was measured locally
• Main Outcome Measures• Composite adverse outcomes of death, intensive care unit
admission, disease-specific complications, or recurrent infection within 30 days
• Antibiotic exposure and adverse effects from antibiotics
52
Schuetz P et al. J Am Med Assoc. 2009;302:1059-66.
53
RATES OF COMBINED ADVERSE OUTCOMES AND MORTALITY BY RANDOMIZATION GROUP
No. (%) of Patients
PCT Control Risk Difference, % Group Group Group (95% CI)
All patients (intention-to-treat) (n = 671) (n = 688)
Overall adverse outcome 103 (15.4) 130 (18.9) −3.5 (−7.6 to 0.4)
Death 34 (5.1) 33 (4.8) 0.3 (−2.1 to 2.5)
ICU admission 43 (6.4) 60 (8.7) −2.3 (−5.2 to 0.4)
Recurrence/rehospitalization 25 (3.7) 45 (6.5) −2.8 (−5.1 to −0.4)
Per-protocol population (n = 633) (n = 650)
Overall adverse outcome 95 (15.0) 123 (18.9) −3.9 (−8.2 to 0.03)
Death 29 (4.6) 31 (4.8) −0.2 (−2.6 to 2.0)
Community-acquired pneumonia (n = 460) (n = 465)
Overall adverse outcome 74 (16.1) 94 (20.2) −4.1 (−9.1 to 0.9)
Death 24 (5.2) 26 (5.6) −0.4 (−3.3 to 2.6)
Schuetz P et al. J Am Med Assoc. 2009;302(10):1059-66.
0
Schuetz P et al. J Am Med Assoc. 2009;302(10):1059-66.
Antibiotic Exposure in Patients Receiving Antibiotic Therapy
All Patients (n = 1359)
Community-acquired Pneumonia (n = 925)
Patie
nts
Rece
ivin
g An
tibio
tic T
hera
py, %
20
40
60
80
100
Time After Study Inclusion, d Time After Study Inclusion, d0 1 2 5 7 9 11 >13
No. of Patients PCT 506 484 410 306 207 138 72 46 Control 603 589 562 516 420 324 157 100
417 410 359 272 161 126 64 41461 453 444 428 361 292 146 91
0 1 2 5 7 9 11 >13
PCTControl
Schuetz P et al. J Am Med Assoc. 2009;302(10):1059-66.
Antibiotic Exposure in Patients Receiving Antibiotic Therapy
0
Patie
nts
Rece
ivin
g An
tibio
tic T
hera
py, %
20
40
60
80
100
Time After Study Inclusion, d0 1 2 5 7 9 11 >13
Time After Study Inclusion, d0 1 2 5 7 9 11 >13
Exacerbation of COPD (n = 228)
Acute Bronchitis (n = 151)
No. of Patients PCT 56 47 30 23 16 6 4 2 Control 79 78 67 56 40 20 5 4
16 11 9 3 3 1 1 141 38 35 19 8 3 0 0
PCT: ProcalcitoinCOPD: Chronic Obstructive Pulmonary Disease
PCTControl
All Patients (n = 1359)
Prop
ortio
n w
ith C
ombi
ned
Adv
erse
Out
com
e
0 10 20 30
0.0
0.1
0.2
Days Since Randomization
No. at Risk
PCTControl
671 605 579 568688 598 576 558
CAP (n = 925)
Prop
ortio
n w
ith C
ombi
ned
Adv
erse
Out
com
e
0 10 20 30
0.0
0.1
0.2
Days Since Randomization
No. at Risk
PCTControl
460 408 394 386465 396 383 371
Adverse Outcomes
PCTControl
Schuetz P et al. J Am Med Assoc. 2009;302(10):1059-66.
57
CONCLUSIONS
• An algorithm with PCT cutoff ranges was noninferior to clinical guidelines in terms of adverse outcomes in CAP:• Reduced antibiotic exposure• Reduced associated adverse effects
• In countries with higher antibiotic prescription rates, PCT guidance may have clinical and public health implications
57
Schuetz P et al. J Am Med Assoc. 2009;302:1059-66.
58
PROCALCITONIN: CASE STUDIES FROM THE EMERGENCY DEPARTMENT
59
CASE STUDY- H.C.
• 31 year old female w/ multiple sclerosis on weekly plasmapheresis
• Hospitalized in early July for possible catheter infection• Catheter removed, only 1 blood culture growing coagulase
negative staph.• Transitioned from vancomycin to ofloxacin then to doxycycline
60
CASE STUDY- H.C.
• Seen in ER June 8 the night of hospital discharge. Patient still concerned about redness and itchiness near former line site
• Given empiric dose of vancomycin after drawing blood cultures, CBC, PCT.
• Discharged home to be followed by PCP and dermatology next day to determine if broad spectrum antibiotics needed to be continued.
• June 9 dermatology clinic visit suggests patient w/ contact dermatitis; continues previous course of doxy
61
CASE STUDY H.C.
• Procalcitonin 0.11• PCT level provides reassurance that:
• recurrence of systemic infection unlikely,• present narrow-spectrum antibiotic choice likely effective providing
better antimicrobial stewardship
62
CASE STUDY E.P.
• “classic” PCT benefit case• 72 yo male w/ valvular heart disease, sick sinus syndrome s/p
pacemaker* to ED w/ acute SOB on July 8th middle of night shift.• Not known to our system, his primary hospital ER was on bypass,
no old records or previous imaging available• O2, bronchodilators, empiric broad spectrum antibiotics after
blood cultures, labs including PCT• Admitted to intermediate care unit for high flow O2, antibiotics,
monitoring, bronchodilators, trial of diuretics.
*increasing prevalence of elderly patients with pacemakers or on betablockers reduces clinical vital sign effectiveness in diagnosis SIRS and Sepsis since heart rate may be artificially blunted
63
CASE STUDY E.P.
• Within 24 hours he required transfer to the ICU and intubation for respiratory distress and sepsis
• PCT was 3.45 from ED draw but due to his nighttime arrival was not available until after admitted to floor.
64
CASE STUDY E.C.
• 63 yo male w/ fever, chills, atrial fibrillation with RVR (HR 140s)• Treated with diltiazem and broad spectrum antibiotics• Symptoms resolved within two days and patient discharged home
on azithromycin• Emergency department PCT was 0.12• Record review show patient's previous admission for afib with
RVR was attributed to documented influenza A• No virology studies during this admission, only "positive"
microbiological finding was a coag negative staph blood culture on hospital day 2.
• Should patient have had virology screening done even though it was not flu season?
65
INFORMATION FROM PCT ADDS TO THE QUALITY OF THE CLINICAL DECISION MAKING
• Understand the kinetics and limitations of any test in order to optimize its utilization!
• Guidance of therapy• Decision on antibiotic initiation• Guidance of duration of therapy
• Risk stratification of patients• Admission to hospital• Admission to ICU• Escalation of therapy
• Guidance of diagnosis• More appropriate selection of who might
need invasive diagnostic tests• Rational utilization of advance imaging
modalities• Improved direction in choice of microbiology
and virology studies
66
THANK YOU!
QUESTIONS?
COMMENTS?