Community acquired pneumonia 2015 part 2

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SAMIR EL ANSARY COMMUNITY ACQUIRED PNEUMONIA 2015 - 2

Transcript of Community acquired pneumonia 2015 part 2

Page 1: Community acquired pneumonia  2015  part 2

SAMIR EL ANSARY

COMMUNITYACQUIREDPNEUMONIA 2015 - 2

Page 2: Community acquired pneumonia  2015  part 2

Global Critical Carehttps://www.facebook.com/groups/1451610115129555/#!/groups/1451610115129555/

Wellcome in our new group ..... Dr.SAMIR EL ANSARY

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What defines a treatment failure?The majority of patients receiving appropriate

therapy show a favorable clinical response within 72 hours.

Therefore initial antibiotic therapy should not be changed before 72 hours unless indicated by significant clinical worsening or microbiologic

data. Remember that certain host factors, such as

advanced age, alcoholism, and chronic obstructive pulmonary disease, have been associated with delayed resolution despite

appropriate treatment.

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What defines a treatment failure?

Radiographic resolution of pneumonia lags behind clinical improvement and in some cases may take up to 8 to 10

weeks to clear completely.

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Discuss the potential reasons why a patient may not respond

favorably to empiric therapy.

Clinical deterioration or a lack of response to empiric antimicrobial

therapy within 3 days often indicates treatment failure, warranting thorough reassessment and

additional investigation.

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1. Inappropriate antimicrobial therapya. Is the dosing adequate?

b. Are all potential bacterial pathogens covered by the empiric regimen?

c. Are the organisms resistant or has a previously sensitive pathogen developed resistance?

d. Is the pathogen bacterial? Consider other pathogens to include viruses, endemic fungi, and

mycobacteria.e. Is the host immunocompromised and at risk for opportunistic infections such as Pneumocystis jiro

veci?f. Is the disease infectious? Has the patient been

misdiagnosed?

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2. Complications of lung infection or hospitalization

a. Has a lung abscess or empyema developed?

b. Does the patient have acute respiratory distress syndrome (ARDS)?

c. Have the bacteria seeded extrapulmonary sites (e.g., endocarditis, septic arthritis,

meningitis)?d. Has the patient acquired a new

nosocomial infection (e.g., urinary tract infection, central line infection, sinusitis)?

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How should a patient with nonresolving pneumonia be evaluated?The clinician should review initial culture

results and sensitivities and collect additional lower respiratory tract and blood

cultures. Broadening empiric therapy may be indicated while awaiting results of

additional testing. All patients should have a repeated chest

radiograph at this time.

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Additional history may reveal HIV risk factors, tick exposure, travel history, or

other diagnostic clues. Further testing, such as a chest computed

tomographic or ultrasound scan, should be directed at the likely cause of treatment

failure. If the procedure can be performed safely, a thoracentesis of a pleural effusion can

exclude a complicated effusion or empyema.

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Bronchoscopy has good diagnostic utility, and specimens should be sent for quantitative bacterial cultures and

sensitivities, as well as for stains and cultures of unusual organisms

(mycobacteria, viruses,endemic fungi, and P. jiroveci ).

If the diagnosis remains elusive, a trial of corticosteroids or a thoracoscopic or open lung biopsy may be considered in

the appropriate clinical setting.

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Noninfectious processes present with signs and symptoms of acute

pneumonia

include ARDS, traumatic pulmonary contusion, pneumonitis resulting from connective tissue

disease (e.g Noninfectious conditions that can mimic acute pneumonia., systemic lupus erythematosus), acute hypersensitivity

pneumonitis, drug-induced pneumonitis, diffuse alveolar hemorrhage (e.g., Goodpasture

syndrome), Wegener granulomatosis, bronchiolitis obliterans .

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Noninfectious processes present with signs and symptoms of acute

pneumonia

Organizing pneumonia, acute interstitial pneumonia (Hamman-Rich syndrome), acute eosinophilic

pneumonia, pulmonary embolism with infarction, atelectasis, chemical pneumonitis (aspiration), and

malignancy (e.g., bronchoalveolar carcinoma, lymphangitic carcinomatosis, Kaposi sarcoma).

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Hospital-acquired pneumonia (HAP), health care associated pneumonia (HCAP), and ventilator-associated

pneumonia (VAP)?

HAP Hospital-acquired pneumonia is defined as pneumonia that occurs 48

hours or more after admission, which was not incubating at the time of admission.

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HCAP {health care associated pneumonia}

Refers to pneumonia that develops in a patient who lives in a nursing home or long-term care facility; undergoes hemodialysis;

has received IV antimicrobial therapy, chemotherapy, or wound care within the

preceding 30 daysor has been hospitalized for at least 2 days

within the preceding 90 days.

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The causative pathogens in these patients are similar to

those responsible for HAP and VAP and are often

Multidrug resistant (MDR).

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VAP: Universally agreed-on diagnostic criteria for VAP do

not exist; however, commonly used criteria include the presence of all of the following:

1. Mechanical ventilation for > 48 hours.2. A new and persistent infiltrate on chest radiograph or ARDS; in the setting of ARDS, it may be impossible to

visualize a new infiltrate on chest radiograph.3. Two of the following three findings:

a. Fever (temperature >38.3" C)b. Leukocytosis or leukopeniac. Purulent tracheal secretions

4. Quantitative cultures of a lower respiratory tract specimen at or above the threshold defined as consistent

with lung infection.The use of clinical criteria alone without microbiologic

data tends to overdiagnose lung infection.

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How do you decide on the initial empiric antibiotic therapy for

HAP,HCAP, or VAP?If the patient has late-onset pneumonia

development (25 days) or risk factors for MDR pathogens, then broad-spectrum antibiotic

therapy is indicated.

If neither of these criteria is met,limited-spectrum antibiotic therapy is appropriate. If HAP, VAP, or HCAP is suspected, disease

severity is not considered in the initial empiric antibiotic decision.

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Risk factors for MDR pathogens causing HAP, HCAP,and VAP?

Riskfactors for MDR causing HAP, HCAP, and VAP include antimicrobial therapy in

the preceding 90 days, current hospitalization of 5 days or more, high frequency of antibiotic resistance in the

community or in the specific hospital unit, immunosuppressive disease

and/or therapy, or presence of risk factors for HCAP

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Risk factors for MDR pathogens causing HAP, HCAP,and VAP?

and/or therapy, or presence of risk factors for HCAP (hospitalization for 2 days or

more in the preceding 90 days,residence in a nursing home or extended-care facility,

home infusion therapy [including antibiotics], long-term dialysis within 30 days, home wound care, family member

with MDR pathogen).

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What initial empiric antibiotic therapy is recommended for HAP, HCAP, or VAP in patients with no known risk factors for

MDR, early onset pneumonia development, and any disease severity?

Recommended antibiotics include ceftriaxone, levofloxacin (moxifloxacin or ciprofloxacin can replace levofloxacin), ampicillin-sulbactam, or ertapenem.

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What initial empiric antibiotic therapy is recommended for HAP, HCAP, or VAP in patients with no known risk factors for

MDR, early onset pneumonia development, and any disease severity?

Potential pathogens include S.pneumoniae, H. influenzae, methicillin-sensitive S. aureus,

and antibiotic-sensitive enteric gram negative bacilli

(Escherichia coli, Klebsiella pneumoniae, Enterobacter, Proteus, Serratia

marcescens).

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What initial empiric antibiotic therapy is recommended for HAP, HCAP, or VAP in patients with

known risk factors for MDR, late-onset disease development, and any disease severity?

Recommended combination antibiotic therapy includes an :

Antipseudomonal cephalosporin(cefepime or ceftazidime)

Antipseudomonal carbapenems(imipenem or Meropenem)

or p-lactam-p-lactamase inhibitor(piperacillin-tazobactam)

plus an antipseudomonal fluoroquinolone (ciprofloxacin or levofloxacin)

or an aminoglycoside(amikacin, gentamicin, or tobramycin).

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What initial empiric antibiotic therapy is recommended for HAP, HCAP, or VAP in

patients with known risk factors for MDR, late-onset disease development, and any

disease severity?

Linezolid or vancomycin should be added if MRSA risk factors are present or there is a

high incidence locally.

Potential MDR pathogens include P. aeruginosa, K. pneumoniae, Acinetobacter

species, and MRSA

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Some specific treatment strategies for MDR Pseudomonas, Acinetobacter, and MRSA VAP?Combination therapy for P. aeruginosa pneumonia

remains controversial. Resistance is mediated partly by multiple efflux

pumps.

Acinetobacter species are most sensitive to the carbapenems, sulbactam, colistin, and

polymyxin.

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More than 85% ofAcinetobacter species isolates are

susceptible to carbapenems, but resistance is increasing because of either integral membrane

protein (IMP)-type metalloenzymes or carbapenemases of the oxacillinase (OXA) type.

MRSA produces a penicillin-binding protein with reduced affinity for p-lactam antibiotics.

Linezolid is an alternative to vancomycin for the treatment of

MRSA VAP.

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Measures which can be taken to decrease the risk of VAP?

1. Avoid intubation when possible, and apply noninvasive positive-pressure ventilation when

appropriate.2. Use orotracheal tubes preferentially over

nasotracheal tubes.3. Minimize the duration of mechanical ventilation

with the aid of weaning protocols.4. Apply continuous aspiration of subglottic

secretions.5. Maintain an endotracheal tube cuff pressure >20

cm H20 to prevent leakage of oropharyngeal secretions containing bacteria into the lungs.

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6. Avoid unnecessary manipulation of the ventilator circuit.

7. Carefully discard contaminated condensate from the ventilator circuit.

8. Keep the head of the bed elevated by 30 degrees.

9. Avoid heavy sedation and paralytics because they impair the patient's ability to cough.

10. It does not appear that sucralfate or therapies that decrease gastric acid increase

the incidence of nosocomial pneumonia.

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When to continue, de-escalate, and discontinue the use of antibiotic treatment

on the basis of clinical response and culture data?

When HAP, VAP, or HCAP is suspected, consider obtaining lower respiratory tract

samples for culture (quantitative or semiquantitative) and

microscopy.

Unless there is both a low clinical suspicion for pneumonia and negative microscopy of

the lower respiratory tract sampleBegin empiric antimicrobial therapy.

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At day 2 and 3, check cultures and assess clinical response

(temperature, white blood cell [WBC] count, chest radiograph, oxygenation, purulent sputum ,hemodynamic changes, and organ function).

If no clinical improvement is seen after 2 to 3 days with negative cultures, search for

other pathogens, complications, diagnoses, or sites of infection.

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If clinical improvement is noted after 2 to 3 days but cultures are negative

consider stopping antibiotics.

If clinical improvement is noted and cultures are positive, de-

escalate antibiotics, and consider treating selected patients for 7 to

8 days and reassess

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How long should you continue antibiotic management for HAP,

HCAP, or VAP?

In a prospective, randomized clinical trial, an 8-day treatment strategy for culture-proved

VAP resulted in a significant decrease in multiresistant bacteria and more antibiotic-free

days with no differences in mortality, ICU length of stay, or mechanical ventilator-free days when

compared with a 15-day regimen.

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A higher rate of recurrence was documented with the 8-day regimen

when the infection was due to Acinetobacter or Pseudomonas

therefore VAP due to these organisms should be treated for 15

days.

Because the infecting pathogens are similar, HAP and HCAP can be treated

similarly.

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Extended therapy(14-21 days) may be

indicated in the setting of Multilobar disease,

Cavitation, Malnutrition, or Necrotizing gram-negative

infection

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SUMMARY1. Treat empirically if pneumonia is clinically

suspected.2. Select the initial empiric therapy on the basis of the current bacteriology and resistance patterns

at each institution. 3. Obtain cultures of respiratory tract specimens

to identify pathogen(s), preferably before initiation of antibiotics.

However, the administration of antibiotic therapy should not be delayed for diagnostic testing.

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4. Narrow the initial antibiotic regimen on the basis of quantitative culture results and clinical

response (de-escalation).

5. Avoid excessive antibiotic use by de-escalating therapy when appropriate and prescribing the

minimal duration of therapy required for efficacy.

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SAMIR EL ANSARYICU PROFESSOR

AIN SHAMSCAIRO

[email protected]

GOOD LUCK

Global Critical Carehttps://www.facebook.com/groups/1451610115129555/#!/groups/1451610115129555/

Wellcome in our new group ..... Dr.SAMIR EL ANSARY