cap dr yuva

8/13/2019 CAP DR YUVA

1/169


2/169

The New Treatment Paradigm Selecting Appropriate Empiric Antibioti


3/169

3

Community Acquired Pneumonia (CAP)

Definition an acute infection of the pulmonary parenchyma

that is associated with clinical symptoms

accompanied by the presence of an acute infiltrateon a chest radiograph, or auscultatory findingsconsistent with pneumonia, in a patient not

hospitalized or residing in a long term care facilityfor > 14 days before onset of symptoms.

Bartlett. Clin Infect Dis 2000;31:347-82.


4/169

4

Pathophysiology

Aspiration of oropharyngeal organisms

Inhalation of infected aerosols Hematogenous spread from extra-pulmonary sites Contiguous spread Direct inoculation


5/169

5


6/169


7/169


8/1698

Pathophysiology

TYPICAL Organisms Streptococcus pneumoniae

Haemophilus influenza

Streptococcus pyogenes Klebsiella pneumoniae

Moraxella catarrhalis

Staph aureus

Enterobacteriaceae/ Gram negative bacilli

Anaerobic organisms (aspiration) Fusobacterium sp. Prevotella sp.


9/1699

Pathophysiology

ATYPICAL Organsims Mycoplasma pneumoniae

Chlamydia pneumoniae

Chlaymida sp. Legionella sp. Respiratory viruses Others


10/16910

Pathophysiology
http://content.nejm.org/content/vol333/issue24/images/large/08t2.jpeghttp://content.nejm.org/content/vol333/issue24/images/large/08t2.jpeg


11/16911

Guidelines for CAP

American Thoracic Society (ATS)Guidelines - Management of Adults with CAP (2001

Infectious Diseases Society of America (IDSA)

Update of Practice Guidelines Management of CAPinImmuno-competent adults (2003)

ATS and IDSA joint effort (we will follow this)

IDSA/ATS Consensus Guidelines on theManagement of CAP in Adults (March 2007)


12/169


13/16913

CAP The Two Types of Presentations

Classical

Sudden onset of CAP High fever, shaking chills Pleuritic chest pain, SOB Productive cough Rusty sputum, blood tinge

Poor general condition High mortality up to 20% in

patients with bacteremia S.pneumoniae causative

Gradual & insidious onset Low grade fever Dry cough, No blood tinge Good GC Walking CAP Low mortality 1-2%; except

in cases of Legionellosis Mycoplasma, Chlamydiae,Legionella, Ricketessiae,Viruses are causative

Atypical


14/16914

CAP Pathogenesis

Inhalation

Aspiration

Hematogenous


15/16915

AgeObesity; Exercise is protective

Smoking, PVD Asthma, COPDImmuno-suppression, HIV

Institutionalization, Old age homes etcDementia

CAP Risk Factors for Pneumonia

ID Clinics 1998;12:723. Am J Med 1994;96:313


16/16916

Community Acquired Pneumonia (CAP)

Epidemiology4-5 million cases annually~500,000 hospitalizations 20% require admission

~45,000 deathsFewest cases in 18-24 yr groupProbably highest incidence in 65 yrs

Mortality disproportionately high in >65 yrsOver all mortality is 2-30%; Hospitalized Pt mort


17/16917

CAP The Pathogens Involved

56%

10%

6%

6%

5%

4%4%

9%S.pneumoniaeH.influenzaChlamydiaLegionella sppS.aureus

MycoplasmaGram Neg bacilliViruses

40-60% - No causative agent identified

2-5% - Two are more agents identified


18/16918

Streptococcus pneumonia(Pneumococcus)

Most common cause of CAP About 2/3 of CAP are due to S.pneumoniaeThese are gram positive diplococciTypical symptoms (e.g. malaise, shaking chillsfever, rusty sputum, pleuritic chest pain, cough)Lobar infiltrate on CXRMay be Immuno suppressed host25% will have bacteremia serious effects


19/169


20/169


21/169

21

S. aereus CAP Dangerous

This CAP is not common; Multi lobar InvolvemenPost Influenza complication, Class IV or VCompromised host, Co-morbidities, ElderlyCA MRSA A Problem; CA MSSA also occursEmpyema and Necrosis of lung with cavitations

Multiple Pyemic abscesses, Septic ArthritisHypoxemia, Hypoventilation, Hypotension commoVancomycin, Linezolid are the drugs for MRSA


22/169

22

CAP Age wise Incidence

0

200

400

600

800

1000

1200

1400

65

# of cases


23/169

23

CAP Age wise Mortality

0

10

20

30

40

50

60

70

80

65

0 0 02

5.7

74.9

# of deaths


24/169


25/169

25

Age > 65Bacteremia (for S. pneumoniae)

S. aureus, MRSA , PseudomonasExtent of radiographic changes

Degree of immuno-suppression Amount of alcohol consumption

CAP Risk Factors for Mortality

ID Clinics 1998;12:723. Am J Med 1994;96:313


26/169

26

CAP Bacteriology in Hospitalized Pts


27/169

27

CAP Evaluation of a Patient

Hx. PE, CXR

No Infiltrate

Alternate Dx.

Infiltrate or Clinicalevidence of CAP

Evaluate needfor Admission

PORT &CURB 65

OutPatient

MedicalWard ICU Adm.


28/169

28

0

20

40

60

80

100

Cough Fever Dyspnea Phlegm Chest Pain

P E R C E N T

Diagnosis of Pneumonia


29/169

29

Diagnostics

Labs CBC

BMP

Imaging CXR

CT scans

Cultures Blood

Sputum

Other tests


30/169


31/169

31

PORT Scoring PSI

Clinical Parameter Scoring

Age in years Example

For Men (Age in yrs) 50

For Women (Age -10) (50-10)

NH Resident 10 points

Co-morbid Illnesses

Neoplasia 30 points

Liver Disease 20 points

CHF 10 points

CVD 10 points

Renal Disease (CKD) 10 points

Clinical Parameter Scoring

Clinical Findings

Altered Sensorium 20 points

Respiratory Rate > 30 20 points

SBP < 90 mm 20 points

Temp < 350 C or > 400 C 15 points

Pulse > 125 per min 10 points

Investigation Findings

Arterial pH < 7.35 30 points

BUN > 30 20 points

Serum Na < 130 20 points

Hematocrit < 30% 10 points

Blood Glucose > 250 10 points

Pa O2 10 points

X Ray e/o Pleural Effusion 10 points

Pneumonia Patient Outcomes

Research Team (PORT)


32/169

32

Classification of Severity - PORT

Predictors Absent

ClassI

70

ClassII

71 90

ClassIII

91 - 130

Class

IV > 130

Class

V


33/169

33

PSI: Mortality in Risk Classes

0

5

10

15

20

25

30

I II (130)

P e r c e n t

Score

Fine et al. New Engl J Med 1997; 336(4):243-250

Outpatients Hospitalised


34/169

34

CAP Management based on PSI Score

PORT Class PSI Score Mortality % Treatment Strategy

Class I No RF 0.1 0.4 Out patient

Class II 70 0.6 0.7 Out patient

Class III 71 - 90 0.9 2.8 Brief hospitalization

Class IV 91 - 130 8.5 9.3 Inpatient

Class V > 130 27 31.1 IP - ICU


35/169

35

CURB 65 Rule Management of CAP

CURB 65ConfusionBUN > 30RR > 30BP SBP


36/169

36

Algorithmic Approach

CAP Patient

< 50 YearsNo

Co-morbidity

No CURB

Class I

Only OP

CURB +

OP / IP/ICU

Class II-V

Co-morbidityPresent

50 Years

PORT

Step 1Step 2 Step 3

Step 4


37/169

37

Who Should be Hospitalized?

Class I and II Usually do not require hospitalizationClass III May require brief hospitalization

Class IV and V Usually do require hospitalization

Severity of CAP with poor prognosis

RR > 30; PaO2/FiO2 < 250, or PO2 < 60 on room air

Need for mechanical ventilation; Multi lobar involvemenHypotension; Need for vasopressors

Oliguria; Altered mental status


38/169

38

CAP Criteria for ICU AdmissionMajor criteria

Invasive mechanical ventilation requiredSeptic shock with the need of vasopressors

Minor criteria (least 3)

Confusion/disorientationBlood urea nitrogen 20 mg% Respiratory rate 30 / min; Core temperature < 36C Severe hypotension; PaO2/FiO2 ratio 250 Multi-lobar infiltratesWBC < 4000 cells; Platelets


39/169


40/169

40

CHEST X RAY


41/169

41

Diagnostics: CXR Findings

Infiltrates Pleural effusions Abscess /Cavities

Bulging fissures Atelectasis Air bronchograms

Other findings PTX Pleural thickening/Scarring Pulmonary edema

Lymphadenopathy/Masses


42/169

42

Diagnostics: CXR Normal CXR

Immunocompromised Dehydrated Early infection

American Journal of Medicine Sept. 2004: 117, 305-11 2706 patients 911 patients with pneumonia and ( )CXR

These patients were older, increased co-morbidities These patients had similar rates of + sputum/blood cultures These patients had a similar mortality


43/169

43

Diagnostics: CXR

Respiratory Medicine May 2006: 100, 926-32 192 patients with pneumonia Excellent IR for lobes involved, extent of infiltrate, pleura

effusion Poor IR for pattern of infiltrate Minimal relation found between cultured pathogens and

radiologic features of infiltrate on CXR


44/169

44

Diagnostics: CT scan

CT scan Alternative diagnoses Unresolved cases

Complications suspected Concerning CXR Treatment failure


45/169

45

In addition to a constellation of suggestive clinical featur

a demonstrable infiltrate by chest radiograph or otherimaging technique, with or without supportingmicrobiological data, is required for the diagnosis ofpneumonia.

Patients with CAP should be investigated for specificpathogens that would significantly alter standard(empirical management decisions, when the presenceof such pathogens is suspected on the basis of clinicaland epidemiologic clues


46/169

46

CAP Value of Chest Radiograph

Usually needed to establish diagnosis

It is a prognostic indicator To rule out other disorders

May help in etiological diagnosis

J Chr Dis 1984;37:215-25


47/169


48/169


49/169

49

Diagnostics: Cultures

Sputum cultures: Recommendations Outpatient

Optional

Inpatient Optional Recommended when result may change therapy

Recommended

ICU admission/Severe CAP Failure of outpatient therapy Cavitary infiltrates (suspect TB) Alcoholism

Severe COPD


50/169

50

CAP Grams Stain of Sputum

Efficiency of test S. pneumoniae H. influenza

Sensitivity 57 % 82 %

Specificity 97 % 99 %

Positive Predictive Value 95 % 93 %

Negative Predictive Value 71 % 96 %

Good sputum samples is obtained only from 39%83% show only one predominant organism


51/169

51

RECOMMENDATIONS

Pretreatment Gram stain and culture ofexpectorated sputum should be performedonly with a good-quality specimen.

Patients with severe CAP, as defined above,

should at least have blood samples drawn forculture, urinary antigen tests for Legionella pneumophila and S. pneumoniae performed,and expectorated sputum samples collectedfor culture.

For intubated patients, an endotrachealaspirate sample should be obtained


52/169


53/169

53

Diagnostics: Cultures Blood Cultures

Yield pathogen 5-15% Blood cultures often do not change management Most commonly isolated organismStreppneumo

High false positive rate Yield of blood cultures decreased by 50% by prior antibio

therapy Optional Recommended

Severe CAP Immunodeficient states (asplenia, liver disease, HIV) Indications for sputum cultures


54/169

54

Pretreatment blood cultures yielded positive results fa probable pathogen in 5% 14% in large series ofnonselected patients hospitalized with CAP.

The yield of blood cultures is, therefore, relatively lowhen management decisions are analyzed, the impacof positive blood cultures is minor.


55/169

55

The most common blood culture isolate in all CAP

studies isS. pneumoniae. Because this bacterial organism is always considered t

be then most likely pathogen, positive blood cultureresults have not clearly led to better outcomes orimprovements in antibiotic selection .

Blood cultures are also indicated when patients have ahost defect in the ability to clear bacteremia


56/169

56

Pathogens Retrieved from Blood Culture

68%

16%

11%5%

S.pneumoniaeEnterobacteriaStaph.aureusOthers


57/169

Procalcitonine and Disease


58/169

58

0 1 2 3 40.001

0.01

0.1

1

10

100

1000 P


59/169

59

Mortality of CAP Based on Pathogen

P. aeruginosa - 61.0 %

K. pneumoniae - 35.7 %

S. aureus - 31.8 %Legionella - 14.7 %

S. pneumoniae - 12.0 %

C. pneumoniae - 9.8 %H. influenza - 7.4 %


60/169

60

Therapy Algorithm CAP

G. Hffken, J. Lorenz, W. Kern, T. Welte, T. Bauer, K. Dalhoff, E. Dietrich, S. Ewig, P. Gastmeier, B. Grabein, E. Halle, M. Kolditz,R. Marre, and H. Sitter. Guidelines of the Paul-Ehrlich-Society of Chemotherapy, the German Respiratory Diseases Society, the

German Infectious Diseases Society and of the Competence Network CAPNETZ for the Management of Lower Respiratory TractInfections and Community-acquired Pneumonia. Pneumologie 64 (3):149-154, 2010.

Diagnosis

Outpatient Care Hospital Admission

Ward ICU

i.v.oral

Pl b ll d S d


61/169

61 Evans GM, Gaisford WF. Lancet 1938;14-19.

Placebo-controlled Study

M th d


62/169

62

Methods

3 9 g/day of M.& B. 693 2( p - Aminobenzenesulphonamido )pyridine

Gram stain White blood cell count

Clinical data

Evans GM, Gaisford WF. Lancet 1938;14-19.


63/169


64/169

64

Traditional Treatment Paradigm

Conservative start with workhorse antibiotics

Reserve more potent drugs for non-responders


65/169

65

New Treatment Paradigm

Hit hard and early with appropriate antibiotic(s)

Short Rx. Duration; De-escalate where possible


66/169

66

Objective 2Objective 1

Avoid emergenceofmultidrug resistantmicroorganisms

Immediate Rx.of patients withserious sepsis

The Therapy Conundrum


67/169

67

Inappropriate therapy (%)

0

30

50

10

CAP

20

40

HAP HAP on CAP

17

34

45

Kollef, et al. Chest 1999;115:462 474

The Effect of the Traditional Approach

f l


68/169

68

Dont Wait for Results !

Switching aftersusceptibility results

p


69/169

69

Risk assessment approachEarly Antibiotic selectionChange treatment driven by localsurveillanceHit hard and hit early

As short a duration as possibleDe-escalate when and where possible

CAP Treatment Consensus


70/169

70

OPAT OP Parenteral Antimicrobial Therapy


71/169

Antibiotic Dosage, Route, Frequency and Duration


72/169

72

Antibiotic Dosage, Route, Frequency and Duration

Doxyclycline 100-200 mg PO/IV BID for 7 to 10 days

Azithromycin 500 mg OD IV 3 days + 500 mg OD PO for 7-10 days

Clarithromycin 250 500 mg BID PO for 7 14 days

Telithromycin 800 mg PO OD for 7 10 days

Levofloxacin 750 mg PO/IV OD for 5 days

Gatifloxacin 400 mg PO or IV OD for 5 to 7 days

Moxifloxacin 400 mg PO or IV OD for 5 to 7 days

Gemifloxacin 320 mg PO OD for 5 7 days

Amoxyclav 2 g of Amoxi +125 mg of Clauv PO BID for 7 to 10 days

Ceftriaxone 2 g IV BID for 3 to 5 days + PO 3G CS

Ertapenum 1 g OD IV or IM for 7 to 14 days

E i i T O i


73/169

73

Empiric Treatment Outpatient

Healthy and no risk factors for DR S.pneumoniae1. Macrolide or DoxycyclinePresence of co-morbidities, use of antimicrobialswithin the previous 3 months, and regions with ahigh rate (>25%) of infection with Macrolideresistant S. pneumoniae1. Respiratory FQ Levoflox, Gemiflox or Moxiflox

2. Beta-lactam (High dose Amoxicillin, Amoxicillin-Clavulanate is preferred; Ceftriaxone, Cefpodoxime,Cefuroxime)plus a Macrolideor Doxycycline

E i i T I i N ICU


74/169

74

Empiric Treatment Inpatient Non ICU

1. A Respiratory Fluoroquinolone (FQ) Levoor2. A Beta-lactamplus a Macrolide (or Doxycycline)

(Here Beta-lactam agents are 3 GenerationCefotaxime, Ceftriaxone, Amoxiclav)

3. If Penicillin-allergic Respiratory FQ or

Ertapenem is another option

E i i T I i i ICU


75/169

75

Empiric Treatment: Inpatient in ICU

1. A Beta-lactam (Cefotaxime, Ceftriaxone,

or Ampicillin-Sulbactam)plus

either Azithromycinor Fluoroquinolone2. For penicillin-allergic patients, a respiratory

Fluoroquinolone and Aztreonam


76/169


77/169

D ti f Th


78/169

78

Duration of Therapy

Minimum of 5 days Afebrile for at least 48 to 72 h

No > 1 CAP-associated sign of clinical instability

Longer duration of therapy

If initial therapy was not active against the identified

pathogen or complicated by extra pulmonary infectio

N d t Th S d f D l ! (Cl 4 5)


79/169

79

New data The Speed of Delay ! (Class 4,5)

0

10

20

30

40

50

60

70

80

90

0.5 1 2 3 4 5 6

Delay in treatment (hours) from hypotension onset

S u r v i v a

l ( % )

Each hour of delay carries7.6% reduction in survival

Kumar, et al. Crit Care Med 2006;34:1589 1596

CAP S f E i i T t t


80/169

80

CAP Summary of Empiric Treatment

Outpatient Rx any one of the three Macrolide or Doxycycline or FluoroquinolonePatients in General Medical Ward 3rd Generation Cephalosporin + Macrolide Betalactum / B-I + Macrolide or B / B-I + FQ Fluroquinolone alonePatients in ICU 3GC + Macrolide or 3GC + FQ B/B-I + Macrolide or B/B-I + FQ

IDSA guidelines: Clin Infect Dis 2000;31:347-82

CAP T t t S


81/169

81

CAP Treatment Summary

CAP Class Site of Care Treatment 1 Treatment 2 Treatment 3

Class I OP AZ CLR ER / Doxy

Class II OP FQ B + M B + Doxy

Class III OP + IP FQ IV I V - B + AZ Aztreo + FQ

Class IV Med Ward FQ + AZ B 3G + AZ Etrap + M

Class V ICU B 3G + AZ B 3G + FQ CarbepenumSulbac ,Tazob

Strategies for Prevention of CAP


82/169

82

Strategies for Prevention of CAP Cessation smoking Influenza Vaccine (Flu shot Oct through Feb)

It offers 90% protection and reduces mortality by 80% Pneumococcal Vaccine (Pneumonia shot)

It protects against 23 types of Pneumococci70% of us have Pneumococci in our RTIt is not 100% protective but reduces mortality Age 19-64 with co morbidity of high for pneumonia Above 65 all must get it even without high risk

Starting first dose of antibiotic with in 4 h & O2 status

Switch to Oral Therapy


83/169

83

Switch to Oral Therapy

Four criteriaImprovement in cough, dyspnea & clinical sig Afebrile on two occasions 8 h apart

WBC decreasing towards normalFunctioning GI tract with adequate oral intake

If overall clinical picture is otherwise favorabl

hemodynamically stable; can switch to oraltherapy while still febrile.

Management of Poor Responders


84/169

84

Management of Poor Responders

Consider non-infectious illnessesConsider less common pathogens

Consider serologic testingBroaden antibiotic therapyConsider bronchoscopy

CAP Complications


85/169

85

CAP Complications

Hypotension and septic shock3-5% Pleural effusion; Clear fluid + pus cells1% Empyema thoracis pus in the pleural space

Lung abscess destruction of lung - CSLDSingle (aspiration) anaerobes,PseudomonasMultiple (metastatic)Staphylococcus aureus

Septicemia Brain abscess, Liver AbscessMultiple Pyemic Abscesses

CAP So How Best to Win the War?


86/169

86

CAP So How Best to Win the War?

Early antibiotic administration within 4-6 hoursEmpiric antibiotic Rx. as per guidelines (IDSA / ATSPORT PSI scoring and Classification of cases

Early hospitalization in Class IV and VChange Abx. as per pathogen & sensitivity patternDecrease smoking cessation - advice / counseling

Arterial oxygenation assessment in the first 24 hBlood culture collection in the first 24 h prior to AbxPneumococcal & Influenza vaccination; SmokingX


87/169

87

NOSOCOMIAL PNEUMONIA


88/169


89/169

Etiology


90/169

90

Etiology

Early vs. Late VAP1 Early onset= Pneumonia develops within 96 hours (4 days

of patient s admission to the ICU or intubation formechanical ventilation

Late onset= Pneumonia develops after 96 hours (4 days) opatient s admission to the ICU or intubation for mechanicalventilation

Very early onset= within 48 hours after intubation21 CDC.gov. Guidelines for preventing health-care-associated pneumonia, 2003.

2 Park DR. The microbiology of ventilator-associated pneumonia.

Nosocomial pneumonia


91/169

91


Mortality and Time of Presentation of HAP


92/169

92

H o s p

i t a

l M o r t a

l i t y ( % )

0

10

20

30

40

50

None Early Onset Late Onset

Nosocomial Pneumonia

P = .504 P


93/169

93


Hence, the importance of focusing on: Accurate diagnosis Appropriate treatment Preventive measures


94/169


95/169


Pathogenesis

Pathogenesis


96/169

96

Microaspiration may occur in up to 45% of healthy volunteduring sleep

Oropharynx of hospitalized patients is colonized with GNR35-75% of patients depending on the severity and type ofunderlying illness

Multiple factors are associated with higher risk of colonizatwith pathogenic bacteria and higher risk of aspiration

Invasion of the lower respiratory tract by:

Aspiration of oropharyngeal/GI organisms Inhalation of aerosols containing bacteria Hematogenous spread

Oropharyngeal colonization


97/169

97

Oropharyngeal colonization

Scannapieco et al showed a transition in the colonization odental plaques in patients in the ICU Control=25 subjects presenting to preventive dentistry clin Study group=34 noncardiac patients admitted to medical

ICU at VA hospital (sampled within 12 hours of admissionand every third day)

Scannapieco et al. Colonization of dental plaque by respiratory pathogensin medical intensive care patients

Colonization of oropharynx


98/169

98

p yMedical ICU (N=34) Dentistry Clinic (N=25)

Species Plaque Mucosa Plaque Mucosa

S. aureus 2 5 0 1

P. aeruginosa 8 7 0 0

K. pneumoniae 2 5 0 0

S. marcescens 3 4 0 0

E. aerogenes 0 0 0 1

E. cloacae 1 1 0 0

E. asburiae 0 0 0 1

P. mirabilis 1 0 0 0

E. coli 0 1 0 0

C. diversus 1 1 0 0 A. calcoaceticus 0 1 0 0

Pasteurella spp. 0 0 1 0

Total 18 24 1 3

Scannapieco et al. Colonization of dental plaque by respiratory pathogensin medical intensive care patients

GI colonization


99/169

99

GI colonization

Increased gastric pH leads to bacterial overgrowth Reflux can then lead to colonization of oropharynx Use of antacids and H2 blockers associated with GI

colonization

Safdar et al. The pathogenesis of ventilator-associated pneumonia:its relevance to developing effective strategies for prevention


100/169

100


101/169


Risk Factors

Etiology- select risk factors forh


102/169

102

pathogensStreptococcus pneumoniae Smoking, COPD, absence of

antibiotic therapy

Haemophilus influenzae Smoking, COPD, absence ofantibiotic therapy

MSSA Younger age, Traumatic coma,Neurosurgery

MRSA COPD, steroid therapy, longerduration of MV, prior antibiotics

Pseudomonas aeruginosa COPD, steroid therapy, longer

duration of MV, prior antibiotics Acinetobacter species ARDS, head trauma,

neurosurgery, gross aspiration,prior cephalosporin therapy

Park DR. The microbiology of ventilator-associated pneumonia.



103/169

103


Risk Factors Host Factors

Extremes of age, severe acute or chronic illnesses,immunosupression, coma, alcoholism, malnutrition, COPD, DM

Factors that enhance colonization of the oropharynx andstomach by pathogenic microorganisms admission to an ICU, administration of antibiotics, chronic lung

disease, endotracheal intubation, etc.



104/169

104


Risk Factors Conditions favoring aspiration or reflux

Supine position, depressed consciousness, endotracheal intubationinsertion of nasogastric tube

Mechanical ventilation Impaired mucociliary function, injury of mucosa favoring bacteri

binding, pooling of secretions in the subglottic area, potentialexposure to contaminated respiratory equipment and contact withcontaminated or colonized hands of HCWs

Factors that impede adequate pulmonary toilet Surgical procedures that involve the head and neck, being

immobilized as a result of trauma or illness, sedation etc.

Risk factors for MDR pa

thogens


105/169

105

Risk factors for MDR pathogens

1.Receipt of antibiotics within the preceding 90 days2.Current hospitalization of 5 days3.Admission from a healthcare-related facility (eg, long-term car

facility, dialysis unit)4.High frequency of antibiotic resistance in the community or in

specific hospital unit5.Presence of risk factors for HCAP including: hospitalization fo

days or more in the preceding 90 days; residence in an extendecare facility; home infusion therapy; chronic dialysis; home wcare; and a family member with an MDR pathogen

6 Immunosuppressive disease and/or therapy

Risk Factors Of VAP In Patienti i M h i l V til ti


106/169

106

receiving Mechanical Ventilation

Age >70 years Chronic lung disease Depressed consciousness Large volume aspiration

Chest surgery Frequent ventilator circuit changes The presence of an intracranial pressure monitor or nasogastric tube H-2 blocker or antacid therapy

Transport from the ICU for diagnostic or therapeutic procedures Previous antibiotic exposure, particularly to third generation cephalosporins Reintubation Hospitalization during the fall or winter season

Mechanical ventilation for ARDS



107/169

107

Etiologic Agents S.aureus Enterobacteriaceae P.aeruginosa Acinetobacter sp. Polymicrobial Anaerobic bacteria

Legionella sp. Aspergillus sp. Viral

Pathogens Associated With HAP


108/169

108

N o s o c o m

i a l P n e u m o n

i a ( % )

0

5

10

15

20

25

30

35

40

PA OSSA ORSA ES SM

P = .003

P = .043

P = .408

P = .985 P = .144

Patho gen

Early-onset NP Late-onset NP

PA = P aerug ino saOSSA = Oxacillin-sensitive

S aureusORSA = Oxacillin-resistant

S aureus

ES = Enterobac te r species

SM = S marcescens

Pathogens Associated With HAP

Ibrahim, et al. Chest. 2000;117:1434-1442.


109/169



110/169

110

Bronchoscopically Directed Techniques for diagnosis of VAPand Quantitative cultures Bronchoscopy with BAL/bronchial brushings (10,000 to 100,000 CFU

and less than 1% of squamous cells)

Protected specimen brush method (>10 CFU/ml)

Protected BAL with a balloon tipped catheter (>5% of neutrophils ormacrophages with intracellular organisms on a Wright-Giemsa stain)



111/169

111

Differential diagnosis ARDS Pulmonary edema Pulmonary embolism Atelectasis Alveolar hemorrhage Lung contusion



112/169

112

Duration of antimicrobial treatment

Optimal duration of treatment has not been established

Most experts recommend 14-21 days of treatment

Recent data support shorter treatment regimens (8 days)


113/169


114/169

114

Treatment of Nosocomial Pneumonia

0369

12151821242730

3336394245

Mortality RecurInfec

P.aerug Abx FreeDays

8days15 days



115/169

115

Preventive Measures Incentive spirometry Promote early ambulation Avoid CNS depressants Decrease duration of immunosupression Infection control measures Educate and train personnel



116/169

116

Preventive Measures Avoid prolonged nasal intubation Suction secretions Semi-recumbent position( 30-45 head elevation) Do not change ventilator circuits routinely more often tha

every 48 hours Drain and discard tubing condensate

Use sterile water for respiratory humidifying devices Subglottic secretions drainage


117/169

117Craven, et al. Chest. 1995;108:s1-s 16.


118/169


119/169

Role of gastric pH(2)


120/169

120

Sucralfate : lower median gastric pH (P < 0.001) and less freqgastric colonization (P = 0.015)

84% late-onset GNB pneumonia have gastric colonization witsame bacteria before pneumonia developed

CONCLUSION: Stress ulcer prophylaxis with sucralfate reducesthe risk for late-onset pneumonia in ventilated patients comparedwith antacid or ranitidine

Decontamination of the digestivetract


121/169

121

tract

preventing oropharyngeal and gastric colonization with aerobiGNB and Candida spp, without disrupting the anaerobic flora

locally administered nonabsorbable antibiotic (eg,polymyxin) andan aminoglycoside or fluoroquinolone + amphotericin B ornystatin.

One RCS showed decrease in pneumonia due to GNB

Decontamination of the digestivetract (2)


122/169

122

tract (2)

A large prospective randomized trial of ICU in the Netherlandt934) :

SDD group lower mortality both in the ICU and duringhospitalization(mortality :15 vs 23% ICU, 24 vs 31 % hospital)

The preventative effects of SDD for HAP have been considerablylower in ICUs with high rates of endemic MDR pathogens

Patient positioning


123/169

123

Several studies supine position vs semirecumbent predisposed to microaspiration of gastric contents

lower incidence of both clinically suspected and microbiologicconfirmed HAP in semirecumbent versus supine patients

No difference in mortality

Suggest : place intubated patients in the semirecumbent positiounless contraindicated.


124/169

Subglottic drainage


125/169

125

Hi-Lo EVAC tube(CASS)

Continuous aspiration of subglotticsecretions (CASS)


126/169

126

secretions (CASS)

Kollef et al. A randomized clinical trial of continuous aspiration ofSubglottic secretions in cardiac surgery patients

Subglottic drainage (2)


127/169

127

Lessen risk of aspiration

5 studies (896 intubated pt) The use of CASS reduced theincidence of VAP by nearly half - risk ratio 0.51 (95% CI 0.37-0.71).

The effect of CASS in limiting VAP was most pronounced ampatients expected to require >72 hours of mechanical ventilati

Via the tube


128/169

128

1) Ventilator circuit changes2) Condensate3) Silver-lined ET tubes

Ventilator circuit management


129/169

129

Craven and colleagues showed that ventilator circuitchange every 24 hours compared to 48 hoursincreased VAP incidence

Several later studies showed that circuit changescould be used safely for greater than 48 hours

Kollef et al. Mechanical ventilation with or without 7-day circuit changes


130/169

Condensate management


131/169

131

Heat-moisture exchanger Theoretical advantage=prevents bacterial colonization of tubing Studies= Mixed results Disadvantage=increases dead space and resistance to breathing

Heated wire to elevate temp of inspired air Advantage=Decreases condensate formation Disadvantage=Blockage of ET tube by dried secretions

CDC.gov. Guidelines for preventing health-care-associated pneumonia, 2003.


132/169


133/169

133

Safety isues of nebulisers in home Safety isues of using nebulisers in in patients and icu Developing guidelines regarding adequate care and

proper usage of nebulisers. Change of tubings and masks.

Silver-lined ET tube


134/169

134

Broad-spectrum antimicrobial activity in vitro Reduces bacterial adhesion to devices in vitro Blocks biofilm formation on the device in animal

models Dog model- decreased severity of lung colonization


135/169

135

1) Baseline2) Wh VAP i li i ll


136/169

136

2) When VAP is clinicallysuspected

3) 3 days later

Am J Respir Crit Care Med2000;162:505

CPIS>6 suggests of pneumonia

Noninfectious causes of fever andl i filt t i VAP


137/169

137

pulmonary infiltrates in VAP

Chemical aspiration without infection (Aspiration pneumoniti Atelectasis

Pulmonary embolism ARDS Pulmonary hemorrhage

Lung contusion Infiltrative tumor Radiation pneumonitis Drug reaction

Diagnosis


138/169

138

Imaging

Gram's stain and culture Bronchoscopy

Gram's stain and culture


139/169

139

unreliable due to contamination with bacteria colonizing theoropharynx The presence ofmany polymorphonuclear leukocytes (and few

epithelial cells) and bacteria, which are morphologically consistenwith bacteria found on culture, improve the predictive power

In addition, the lack of isolation of a pathogen (eg, MRSA orPseudomonas) from a well-collected and adequate expectoratesputum sample can be used to narrow the antimicrobial regime

Blood cultures are extremely helpful when positive, but the yilow


140/169

Bronchoscopy


141/169

141

Protected brush specimen (PBS)

Using a threshold of>103

colony forming units (CFU)/mL sensitivity : 64 to 100 % specificity : 60 to 100 %

Bronchoalveolar lavage (BAL)

Quantitative cultures using a threshold of>104 CFU/mL sensitivity : 72 - 100 % specificity : 69 - 100 %

At least 4 studies concluded that bronchoscopically directed techniques werenot more accurate for diagnosis of VAP than clinical and X-ray criteria,combined with cultures of tracheal aspirate

Therefore no old standard criteria exist

Initial Antibiotic Therapy


142/169

142

Inappropriate therapy is a major risk factor for excessmortality and length of stay in patients with HAP, andantibiotic resistant organisms are the pathogens mostcommonly associated with inappropriate therapy.

In selecting empiric therapy for patients who have

recently received an antibiotic use an agent from adifferent antibiotic class , since recent therapy increasesthe probability of inappropriate therapy and canpredispose to resistance to that same class of

antibiotics .

Initial Antibiotic Therapy


143/169

143

Initial antibiotic therapy should be given promptly sincedelays in administration may add to excess mortality inVAP.

Initial empiric therapy is more likely to be appropriate ifa protocol for antibiotic selection is developedbutadapted to local patterns of antibiotic resistance, witheach ICU collecting this information, and updating it on aregular basis.


144/169

144 TABLE 3. INITIAL EMPIRIC ANTIBIOTIC THERAPY FOR HAP OR VAP IN PATIENTSWITH NO KNOWN RISK FACTORS FOR MDR PATHOGENS, EARLY ONSET, ANDANY DISEASE SEVERITY

Potential Pathogen Recommended Antibiotic*


145/169

145

Potential Pathogen Recommended Antibiotic

Streptococcus pneumoniae Ceftriaxone

Haemophilus influenzae or

Levofloxacin, moxifloxacin, or ciprofloxacin

Methicillin-sensitive Staphylococcus aureus or

Antibiotic-sensitive enteric gram-negative bacilliEscherichia coli Ampicillin/sulbactam

Klebsiella pneumoniae or

Enterobacter species Ertapenem

Proteus species

Serratia marcescens

* See Table 5 for proper initial doses of antibiotics.

The frequency of penicillin -resistant S. pneumoniae and multidrug-resistant S. pneumoniae is increasing; levofloxacin ormoxifloxacin are preferred to ciprofloxacin and the role of other new quinolones, such as gatifloxacin, has not been established.

TABLE 4. INITIAL EMPIRIC ANTIBIOTIC THERAPY FOR HAP OR VAP IN PATIENTS WITHLATE-ONSET DISEASE OR RISK FACTORS FOR MDR PATHOGENS, AND ANY DISEASESEVERITY

Potential Pathogen Combination Antibiotic Therapy*


146/169

146

Pathogens listed in Table 3 and Antipseudomonal cephalosporin

MDR pathogens (cefepime, ceftazidime)

Pseudomonas aeruginosa orKlebsiella pneumoniae (ESBL) Antipseudomonal carbepenem

Acinetobacter species (imipenem or meropenem) or

Lactam/-lactamase inhibitor(piperacillin tazobactam)

plus Antipseudomonal fluoroquinolone (ciprofloxacin or levofloxacin)

or Aminoglycoside

(amikacin, gentamicin, or tobramycin)

plus

Methicillin-resistant Staphylococcus aureus (MRSA) Linezolid or vancomycin

Legionella pneumophila * Initial antibiotic therapy should be adjusted or streamlined on the basis of microbiologic data and clinical response to therapy. If an ESBL strain, such as K. pneumoniae , or an Acinetobacter species is suspected, a carbepenem is a reliable choice. If L. pneumophila is suspected, thecombination antibiotic regimen should include a macolide (e.g., azithromycin) or a fluoroquinolone (e.g., ciprofloxacin or levofloxacin) should be used ratherthan an aminoglycoside. If MRSA risk factors are present or there is a high incidence locally.

Optimal Antibiotic Therapy


147/169

147

Empiric therapy of patients with severe HAP or VAP requires theuse of antibiotics at optimal doses to assure maximum efficacy.

Initial therapy should be administered to all patientsintravenously, with a switch to oral/enteral therapy in selectedpatients with a good clinical response and a functioning intestinaltract. Highly bioavailable agents, such as the quinolones andlinezolid, may be easily switched to oral therapy in such patients.

Aerosolized antibiotics have not been proven to have value inthe therapy of VAP.

Optimal Antibiotic TherapyCombination therapy should be used if patients are likely to be


148/169

148

infected with MDR pathogens. No data have documented thesuperiority of this approach to monotherapy, except to enhance thelikelihood of initially appropriate empiric therapy.

If patients receive combination therapy with an aminoglycosidecontaining regimen, the aminoglycoside can be stopped after 5-7days in responding patients.

Monotherapy with selected agents can be used for patients with

severe HAP and VAP in the absence of resistant pathogens.Patients in this risk group should initially receive combination therapyuntil the results of lower respiratory tract cultures are known andconfirm that a single agent can be used.

Optimal Antibiotic Therapy


149/169

149

MRSA pneumonias:

- prolonged intubation periods- prior use of antibiotics

Pseudomonas aeruginosa pneumonias:- structural pulmonary disease

- 1 week of prior hospitalization- prolonged periods of intubation (>5 days) - prior exposure to antibiotics

A. Baumannii VAP:- neurosurgery- ARDS- head trauma- large-volume pulmonary aspiration.

Combinationpiperacillin/tazobactam + ciprofloxacin ,

oramikacin + imipenem, meropenem or anantipseudomonal cephalosporin.

carbapenems, sulbactam,tigecycline, colistin

linezolid

Duration of antimicrobial treatment


150/169

150

Optimal duration of treatment has not beenestablished

Most experts recommend 14-21 days of treatment

Recent data support shorter treatment regimens (8days)

Comparison of 8 vs.15 days of antibiotics for VAP


151/169

151

Prospective, randomized, double blind clinical trial51 French ICUs401 patients with VAP (quantitative culture results)

Clinical effectiveness comparable, with the possibleexception of VAP caused by non fermenting GNR

JAMA 290 No 19, November 2003


152/169

152

Non resolving pneumonia


153/169

153

Non resolving pneumonia is a clinicalsyndrome in which focal infiltrates beginwith some clinical association of acutepulmonary infection and despite a minimum

of 10 days of antibiotic therapy patientseither dont improve or worsen orradiographic opacities fail to resolve within12 week


154/169

Normal CXR & Pneumonic Consolidation


155/169

155

Lobar Pneumonia S.pneumoniae


156/169

156

CXR PA and Lateral Views


157/169

157


158/169

Lobar Pneumonia


159/169

159

Special forms of Consolidation


160/169

160


161/169

Special Forms of Pneumonia


162/169

162

Special Forms of Pneumonia


163/169

163

Complications of Pneumonia


164/169

164


165/169


166/169

Mycoplasma Pneumonia


167/169

167

Chlamydia Trachomatis


168/169

168

Rare Types of Pneumonia


169/169

cap dr yuva

Documents