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healthcare-associated pneumonia
since guidelines have been released, several studies have evaluated these criteria
no clear benefit in patient outcome
poorly predicted patients with multi drug resistant (MDR) pathogens
resulted in 15 years of antibiotic over-prescribing
despite recommendations to abandon this definition, it’s still often used to justify broad therapy
pathophysiology of pneumonia
microbes invade the airway
through inhalation, aspiration, or even contamination from food
host defenses are overcome
impaired mucociliary clearance
overwhelmed or absent macrophages
bacterial proliferation and inflammation
bacteria invade alveoli
macrophages recruit neutrophils and produce cytokines
the immune system is ‘ramped up’
signs and symptoms of pneumonia
new or worsening sputum production
new or worsening cough
increased respiratory rate
pleuritic chest pain
leukocytosis or leukopenia
fever/hypothermia
asculatory changes, such as crackles or rales
decreases in oxygenation
diagnosis of pneumonia
chest x-ray (CXR) is essential
however, it doesn’t differentiate between viruses and bacteria
infiltrate/consolidation on CXR may represent pneumonia
doesn’t differentiate between bacteria and viral
CXR is also not specific to pneumonia
if a CXR clears up overnight → rule out pneumonia
for patients that are hospitalized with a negative CXR but positive clinical symptoms, it’s reasonable to re-image in 24-48 hours
sputum analysis
in the majority of patients, cultures are conducted based on expectorated sputum (“gunk” in the lungs)
40-60% of patients will not produce sputum
40-60% of those that can → poor samples
a “good” sample requires identification of polymorphonuclear leukocytes (PMNs) and lack of epithelial cells in sputum culture
> 25 PMNs and < 10 epithelial cells
indicated spit and not “gunk”
PMNs indicates inflammation, and thus infection
cultures are recommended in patients with:
severe disease (eg. ICU)
receiving MRSA/P. aeruginosa coverage
procalcitonin test (PCT)
normally produced in thyroidal C-cell
upregulated production in adipocytes response to bacterial infection
a lab test indicative of infection, but anything that has a strong inflammatory response could lead to a false positive
the most commonly used cutoff is 0.25 ng/mL
> 0.25 → antibiotic therapy is encouraged
typically peaks within 24 hours of infection onset
initial elevations may be observed with viral infections, though this is typically followed by a rapid decrease
plays an unclear role in the treatment of CAP
may not be elevated in patients with atypical bacteria
NOT recommended as a guide for initiating antibiotics in patients with radiographically confirmed pneumonia and clinical signs/symptoms
pneumonia severity index (PSI)
determines the treatment setting based on demographics, co-morbidities, phsyical exam, labs, etc
replaced the CURB-65 tool
criteria:
respiratory rate ≥ 30 bpm
SBP < 90 mmHg
temp ≥ 40 or < 35 ºC
tachycardia ≥ 125 bpm
arterial pH < 7.35
BUN ≥ 30 mg/dL
sodium < 130 mmol/L
glucose ≥ 250 mg/dL
Hct < 30%
pO2 < 60 mmHg
PSI risk class 1
< 50 points
outpatient setting
PSI risk class 2
51-70 points
outpatient setting
PSI risk class 3
71-90 points
outpatient or brief inpatient setting
PSI risk class 4
91-130 points
inpatient setting
PSI risk class 5
> 130 points
inpatient setting
CURB-65 criteria
confusion
uremia (BUN > 20 mg/dL)
RR > 30 bpm)
BP < 90/60
age > 65
CURB-65 score 0-1
outpatient setting
CURB-65 score 3
inpatient → floor setting
CURB-65 score ≥ 3
inpatient → ICU setting
IDSA severity criteria
determines whether a not a patient should be admitted to the ICU for their pneumona infection
in combination with clinical judgement, should be used to determine inpatient setting of care (ICU vs non-ICU)
comprised of values that are readily available for patients being admitted
patient must meet 1 major criteria OR 3 minor criteria in order for ICU admission
IDSA severe pneumonia: minor criteria
need 3:
RR ≥ 30 bpm
PaO2/FiO2 ≤ 250
multilobal infiltrates
confusion
BUN ≥ 20 mg/dL (uremia)
leukopenia due to infection → WBC < 4×103
thrombocytopenia → platelets < 100×103
hypothermia (< 36ºC)
hypotension requiring aggressive fluid resuscitation
IDSA severe pneumonia: major criteria
need 1:
mechanical ventilation
septic shock (requires vasopressors)
bacteria that can cause CAP
Streptococcus pneumoniae → most common
Haemophilus influenzae
Mycoplasma pneumoniae
Clamydophilia pneumoniae
Legionella pneumophila
S. aureus (rare, may have risk factors for infection)
rarely other gram-negative bacilli
etiology of CAP
often no pathogen is identified (up to 62%)
viral pathogens account for 24% of identified pathogens
bacterial pathogens account for 14% of CAP infections
normally, treat as bacterial infection
viral infections → tend to not have to treat
risk factors for MRSA and P. aeruginosa
overall, CAP caused by these pathogens is rare
prevalence of these pathogens should be locally evaluated
most consistent factors:
previous infection with MRSA or P. aeruginosa, especially respiratory infections
hospitalization WITH receipt of intravenous antibiotics witihn 90 days
MRSA in the community
often severe production of Panton Valentin Leukocidin plays a role in cavitary pneumonia
still, very uncommon
first-line agents for outpatients (otherwise healthy)
options:
amoxicillin
doxycycline
alternative agents for outpatients (otherwise healthy)
options:
azithromycin
clarithromycin
if local S. pneumoniae resistance is < 25%
first-line agents for outpatients WITH co-morbidities
options:
amoxicillin/clauvanate
cefpodoxime
cefuroxime
PLUS
azithromycin
doxycycline
so for example, a regimen would look like cefpodoxime + cefuroxime
these regimens are used because these patients are at higher risk for resistant organisms
alternative agents for outpatients WITH co-morbidities
options
levofloxacin
moxifloxacin
remember, ciprofloxacin is NOT a respiratory antibitotic
fluoroquinolones and macrolides
remember, these agents can cause QTc prolongation, and as such, should be used with caution and avoided if possible
in patients with contraindications to these agents, doxycycline can be used alternatively
first-line agents for non-ICU inpatients with NO MRSA/P. aeruginosa risk factors
options:
IV ß-lactam + azithromycin
alternative agents for non-ICU inpatients with NO MRSA/P. aeruginosa risk factors
options:
levofloxacin
moxifloxacin
IV ß-lactam + doxycycline
first-line agents for non-ICU inpatients with recent antibiotic exposure
options:
IV ß-lactam + azithromycin
first-line agents for non-ICU inpatients with recent MRSA infection
options:
add MRSA coverage to CAP regimen
first-line agents for non-ICU inpatients with recent P. aeruginosa infection
options:
change IV ß-lactam to anti-pseudomonal IV ß-lactam (cefepime)
IV ß-lactams
options:
ceftriaxone
ceftaroline
cefotaxime
ampicillin-sulbactam
first-line agents for ICU inpatients with NO MRSA/P. aeruginosa risk factors
options:
IV ß-lactam + azithromycin
alternative agents for ICU inpatients with NO MRSA/P. aeruginosa risk factors
options:
IV ß-lactam + levofloxacin OR moxifloxacin
first-line agents for ICU inpatients with MRSA/P. aeruginosa risk factors
options:
vancomycin + anti-pseudomonal ß-lactam
linezolid + anti-pseudomonal ß-lactam
MRSA coverage
patients receiving MRSA/P. aeruginosa coverage can be safely de-escalated at 48 hours if cultures are not positive for that organism
additionally, MRSA therapy can be discontinued with negative MSRA nasal PCR
MRSA nasal PCR
detects nasal colonization of S. aureus
it’s an excellent negative predictor of MSRA pneumonia
negative result = unlikely MRSA infection and can safely discontinue MRSA therapy
however, it’s a poor positive predictor
positive result = idk bruh
no need to escalate therapy, can just continue
additional diagnostic testing
pneumococcal urinary antigen test generally is not recommended
only in patient with severe pneumonia (ie. in the ICU)
Legionella urinary antigen test is generally not recommended either, except:
patients with severe (ICU) pneumonia
indicated by epidemiologic factors such as local outbreak or recent travel
most patients coming from the community won’t have this, but if it’s becoming more prevalent in a nursing home population, there’s an issue
pneumococcal urinary antigen test
detects portion of the cell wall of bacteria
high specificity (>94%) with varied sensitivity (>65%)
predictive values increase with bacteremia
Legionella urinary antigen test
a specific antigen immunoassay
only detects serotype 1 (most common serotype)
upp to 99% specificity
may persist following adequate treatment (weeks to months)
Legionella pneumophilia infection
increasing in prevalence in recent years
generally results from environmental exposures (eg. contaminated water systems)
may be associated with:
muscle aches
non-productive cough
rapid progression
high fevers
CXR typically shows patchy infiltrates or nodular infiltrates
frequently, these patients have a severe presentation
aspiration pneumonia/pneomonitis
the entry of something other than air into the lungs, eg spit or even food
occurs more commonly in elderly and patients admitted from nursing homes/long-term care facilities
difficult to distinguish between pneumonia and pneumonitis
inflammation without infection
treatment does NOT require additional anaerobic coverage beyond a typical CAP regimen
mouth anaerobes are typically gram-positive and respond to ß-lactams
treatment duration
generally, 5-7 days is appropriate (unless there’s resistance, or slow to improve)
patient should be afebrile for 48-72 hours prior to discontinuation of antibiotics
FQs and macrolides should NOT exceed 5 days of treatment!
new data suggests that treatment as short as 3 days may be appropriate for some patients
HAP/VAP guidelines recommend no more than 7 days unless patients are not responding to treatment
3-day treatment
suitable for patients that are not critically ill, immunocompetent, and clinically stable after 3 days of ß-lactam treatment
key exclusions:
aspiration pneumonia
legionellosis
atypical pathogens
lung abscess
massive pleural effusion
directed therapy
often, no pathogen is identified, and empiric therapy is continued for the duration
culturing is not super helpful most of the time → just continue with empiric therapy
this type of treatment approach is based on susceptabilities, when available
for Legionella: lexofloxacin or azithromycin
recently approved drugs for CAP
lefamulin
omadacycline
delafloxacin
these agents appear to be effective for PORT class 4
has a potential role for patients with allergies/intolerance to other agents
have high rates of susceptibility for common CAP pathogens
much more expensive