1. procalcitonin: Advancing Decision Making in sepsis
Sean-Xavier Neath, M.D., Ph.D.
Assistant Clinical Professor of Medicine
Department of Emergency Medicine
University 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 Scientific
BRAHMS
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:

6. Sepsis: ACCP/SCCM Definitions
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
The American College of Chest Physicians (ACCP) and Society of Critical Care Medicine (SCCM) held a consensus conference in August 1991 to agree on a set of definitions that could be applied to patients with sepsis and organ dysfunction. The consensus panel also recommended the use of severity scoring methods to characterize the disease and develop a comprehensive model for the syndrome.
This slide provides a brief definition of the various components of the sepsis syndrome. Notably, this is a non-linear process rather than a continuum, and the presence of organ dysfunction identifies a population with a significant risk of mortality.
Bone RC, Balk RA, Cerra FB, et al. Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Chest 1992;101:
ACCP/SCCM Consensus Statement. Chest. 1992;101:1644.

7. SIRS Infection Sepsis Parasite Severe Sepsis Trauma Bacteria Burns
Virus
SIRS
Sepsis
Fungus
shock
Trauma
Severe
SIRS
Bacteria
BSI
Burns
Adapted from SCCM ACCP Consensus Guidelines

8. Population Adjusted Incidence of Sepsis (USA)
Martin GS et al. NEJM 2003;348:1346

9. Cases of Sepsis by Pathogen (USA)
Martin GS et al. NEJM 2003;348:1346

10. Infection Source in Severe Sepsis
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, Critical Care Med

13. Difficulties in Diagnosis and Treating Sepsis in the Emergency Department
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

14. Difficulties in Diagnosis and Treating Sepsis in the Emergency Department
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

15. Duration of hypotension before initiation of effective antimicrobial therapy is the critical determinant of survival in human septic shock
Kumar A. et al., Crit Care Med 2006, 34:1286

16. Failure to Intervene Quickly Can Be Fatal
N=511 over 7 yrs. 2.5 years before MET and 5 yrs after MET. Before/after study design
Time to shock alert = RRT activation
Sebat CCM 2007; 35: 2568

17. Key Areas of Sepsis Management
Initial Resuscitation
Diagnosis
Antibiotic therapy
Source Control
Fluid therapy
Vasopressors
Inotropic Therapy
Steroids
Recombinant Human Activated 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
This index list also provides a means to quickly link to the specific slides related to the topic. Click on the subject when the slide is in the “show” mode and the slides automatically advances to the first slide of that specific guideline.
Dellinger, et. al. Crit Care Med 2004, 32:

18. Role of Procalcitonin in initial Sepsis management

19. Why Procalcitonin?
Integrated use of PCT with other clinical and laboratory information permits:
Increased accuracy of clinical diagnosis of relevant bacterial infection / sepsis
Improved clinical decision making and patient management

20. Procalcitonin – A biomarker for the assessment of critically ill patients at risk for severe bacterial infection and sepsis
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
Morgenthaler N. et al., Clin Lab 2002, 48:

21. Procalcitonin – normally an intermediate product in the synthesis of Calcitonin
Thyroid
After P. Linscheid, Endocrinology 2003
Site of synthesis for PCT in healthy persons are the C-cells of the thyroid. Expression of CT-mRNA takes place only in the neuroendocrine cells. Release occurs in the form of the posttranslational processed hormone
Calcitonin enclosed in Golgi vesicles. This hormone plays an important role in the pathway and regulation of calcium and phosphate in the bone metabolism.
N-Pro
Calcitonin
Katacalcin N C 1
57 60
91 96
116
LOW PCT values in the blood of healthy persons: pg/ml (97.5 percentile); median = 12.7 pg/ml*
Morgenthaler N. et al., Clin Lab 2002, 48:

22. Procalcitonin – Presence of Bacterial Infection Stimulates PCT Production
Linscheid et al described the mechanism of the biochemical pathway and site of synthesis of PCT after bacterial infection. They investigated which factors affected the synthesis. Results show that in case of bacterial infection two mechanisms of synthesis are at work.
At first cytokine-stimulated adherent monocytes release PCT in low quantities (<2h). This synthesis is limited. But it plays an important role in the initiation of PCT synthesis in storage tissues of humans. This PCT burst is initiated in all storage tissues (>18h). Parenchymal tissue is the most common type of tissue in the human organism. This explains why extreme concentrations of PCT can be generated ( fold increase in contrast to physiological concentrations). The PCT burst continues as long as the stimulus for synthesis exists.
In additional experiments it was clarified why PCT is only synthesized during bacterial but not in viral infections. Cells were incubated on one hand with IL-1β and on the other hand with IL-1β and INF-γ.
The results showed that cells treated with both cytokines do not synthesize PCT. The conclusion was that cells infected by viruses released INF-γ. This cytokine has a direct influence on the synthesis of PCT. These findings led to the explanation of the fact that PCT is a perfect tool to differentiate between viral and bacterial infections (e.g. Gendrel et al. 1999).
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
Adapted from Christ-Crain et al. 2005

23. Highly specific induction and release of PCT due to bacterial infection
Calcitonin:
Sources of
production
in healthy
people
Healthy
Sepsis
PCT:
Sources of
Production
in Septic
Patients
In bacterial infection, PCT is produced and released into circulation from the entire body
Müller B. et al., JCEM 2001

24. PCT Level Increase = Increased Significance of Bacterial Infection
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

25. Highly specific induction and release of PCT due to bacterial infection
Linscheid et al described the mechanism of the biochemical pathway and site of synthesis of PCT after bacterial infection. They investigated which factors affected the synthesis. Results show that in case of bacterial infection two mechanisms of synthesis are at work.
At first cytokine-stimulated adherent monocytes release PCT in low quantities (<2h). This synthesis is limited. But it plays an important role in the initiation of PCT synthesis in storage tissues of humans. This PCT burst is initiated in all storage tissues (>18h). Parenchymal tissue is the most common type of tissue in the human organism. This explains why extreme concentrations of PCT can be generated ( fold increase in contrast to physiological concentrations). The PCT burst continues as long as the stimulus for synthesis exists.
In additional experiments it was clarified why PCT is only synthesized during bacterial but not in viral infections. Cells were incubated on one hand with IL-1β and on the other hand with IL-1β and INF-γ.
The results showed that cells treated with both cytokines do not synthesize PCT. The conclusion was that cells infected by viruses released INF-γ. This cytokine has a direct influence on the synthesis of PCT. These findings led to the explanation of the fact that PCT is a perfect tool to differentiate between viral and bacterial infections (e.g. Gendrel et al. 1999).
IFN- released in viral infection, blocks the activation of PCT production, therefore in viral infection PCT levels remain normally low
Adapted from Christ-Crain et al. 2005

26. Benefits and limitations of other Sepsis diagnostic tools
Microbiology (Blood Culture)
Standard of care, time to result, ?Sens., ? Spec.
Availability, costs, variability of source detection
Imaging (X-Ray, Hr-CT)
Molecular Biological Testing
Availability, costs, time to results
Biopsy
Invasive, relatively expensive
Easy to measure, not invasive, relatively inexpensive
Biomarker Testing (PCT)
Slow kinetics , high impact of inflammation (specificity), suppressed by corticosteroids, relatively inexpensive
C-Reactive Protein (CRP)

27. Diagnostic accuracy of PCT compared to other biomarkers used in sepsis
Sensitivity: 89%
Specificity: 94%
NPV: 90% / PPV: 94%
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
Simon L. et al. Clin Infect Dis. 2004; 39:

28. Adding PCT results to clinical assessment improves the accuracy of the early clinical diagnosis of sepsis
AUC with PCT: 0.94
AUC without PCT: 0.74
When PCT is used as a reference, the sensitivity and specificity of sepsis diagnosis can be significantly increased compared with conventional clinical parameters.
Harbarth S et.al. AM J Resp Crit Care Med. 2001; 164:

29. PCT levels increase according to severity of sepsis
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
Harbarth S et al. Am J Respir Crit Care Med 2001, 164: ; Meisner M et al., Critical Care 1999, 3(1): ; Krüger S. et al., Eur Respir J 2008; 31: 349–355

30. 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
PCT used in early detection of infection after liver transplantation – differentiation from rejection
Kuse ER et al., Crit Care Med 2000; 28:

31. PCT kinetics provide important information on prognosis of sepsis patients
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
Brunkhorst FM et al., Intens. Care Med (1998) 24:

32. Interpreting Procalcitonin values

33. PCT release in the absence of infection
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.

34. Adding PCT results to clinical assessment improves the accuracy of the early clinical diagnosis of sepsis in Neonates
UNINFECTED
INFECTED
PCT
(ng/ml)
PCT
(ng/ml)
Time (hours)
Time (hours)
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.
C Chiesa et al. CID 1997

35. Low PCT levels in the presence of bacterial infection may occur:
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. Interpretation of PCT levels
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)

37. PCT kinetics after an infectious challenge
Brunkhorst FM et al., Intens. Care Med (1998) 24:
What is so special about PCT?
Highly specific induction due to bacterial infection
Rapid increase (more rapid compared to CRP)
Correlation to severity of disease
Enormeous magnitude of elevation that can be reached (up to 105 compared to healthy; other parameters: magnitude fold )
Half life of ~24 h
Can be used also in patients with renal insufficiency
Easy to measure
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
Brunkhorst FM et al., Intens. Care Med (1998) 24:

38. PCT reflects the response of the organism to the bacterial challenge
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

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. PCT levels predict bacteremia in patients with community acquire pneumonia (CAP)
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.
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
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 predict bacteremia in patients with community acquire pneumonia
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.
Muller et al. CHEST July 2010

45. Procalcitonin correlates to the severity of the infection/sepsis
Organ Dysfunction
Pneumonia
Harbarth S et al. Am J Respir Crit Care Med 2001, 164:
Meisner M et al., Critical Care 1999, 3(1): 45-50
Krüger S. et al., Eur Respir J 2008; 31: 349–355

46. PCT results provide important information on prognosis of CAP patients in emergency room
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).
Huang, et.al., Annals of Emergency Medicine, Vol 51, March 2008

47. Serial measurement of PCT provides a clearer picture of the patient’s response to antibiotic treatment.
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
Stueber, F. University of Bonn, Lecture at ISICEM, Brussels 2001

48. PCT guidance in antibiotic usage Effects on length of stay
Effect of PCT-guided management in patients with sepsis on ICU length of stay
Nobre V. et alAM Resp Crit Care Med 2008: 177:

49. Pct Guidance on effect on length of icu stay
Effect of PCT-guided management in patients with sepsis on ICU length of stay
Nobre V. et alAM Resp Crit Care Med 2008: 177:

50. PCT guidance in antibiotic usage has been shown to significantly shorten the time patients need to be on antibiotics
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
Nobre V. et al AM Resp Crit Care Med 2008: 177:

51. Schuetz P et al. J Am Med Assoc. 2009;302:1059-66.
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
Effect of Procalcitonin-Based Guidelines vs. Standard Guidelines on Antibiotic Use in Lower Respiratory Tract Infections: The ProHOSP Randomized Controlled Trial
Schuetz P et al. J Am Med Assoc. 2009;302:

52. Schuetz P et al. J Am Med Assoc. 2009;302:1059-66.
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
Schuetz P et al. J Am Med Assoc. 2009;302:

53. PCT Control Risk Difference, % Group Group Group (95% CI)
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 (15.4) (18.9) −3.5 (−7.6 to 0.4)
Death (5.1) (4.8) (−2.1 to 2.5)
ICU admission (6.4) (8.7) −2.3 (−5.2 to 0.4)
Recurrence/rehospitalization (3.7) (6.5) −2.8 (−5.1 to −0.4)
Per-protocol population (n = 633) (n = 650)
Overall adverse outcome (15.0) (18.9) −3.9 (−8.2 to 0.03)
Death (4.6) (4.8) −0.2 (−2.6 to 2.0)
Community-acquired pneumonia (n = 460) (n = 465)
Overall adverse outcome (16.1) (20.2) −4.1 (−9.1 to 0.9)
Death (5.2) (5.6) −0.4 (−3.3 to 2.6)
Schuetz P et al. J Am Med Assoc. 2009;302(10):

54. Antibiotic Exposure in Patients Receiving Antibiotic Therapy
PCT Control
All Patients (n = 1359)
Community-acquired Pneumonia (n = 925)
100 80
Patients Receiving Antibiotic Therapy, % 60 40 20
>13
>13
Time After Study Inclusion, d
Time After Study Inclusion, d
No. of Patients PCT Control
Schuetz P et al. J Am Med Assoc. 2009;302(10):

55. Antibiotic Exposure in Patients Receiving Antibiotic Therapy
PCT Control
Exacerbation of COPD (n = 228)
Acute Bronchitis (n = 151)
100 80
Patients Receiving Antibiotic Therapy, % 60 40 20
>13
>13
Time After Study Inclusion, d
Time After Study Inclusion, d
No. of Patients PCT Control
PCT: Procalcitoin COPD: Chronic Obstructive Pulmonary Disease
Schuetz P et al. J Am Med Assoc. 2009;302(10):

56. Adverse Outcomes PCT Control All Patients (n = 1359) CAP (n = 925) 0.2
Proportion with Combined
Adverse Outcome
0.1
Proportion with Combined
Adverse Outcome
0.1
0.0
0.0 10 20 30 10 20 30
Days Since Randomization
Days Since Randomization
No. at Risk
No. at Risk
PCT
671
605
579
568
PCT
460
408
394
386
Control
688
598
576
558
Control
465
396
383
371
Schuetz P et al. J Am Med Assoc. 2009;302(10):

57. Schuetz P et al. J Am Med Assoc. 2009;302:1059-66.
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
Schuetz P et al. J Am Med Assoc. 2009;302:

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?