PI 1 Flashcards
classification of PNA
causative pathogenic organism
anatomic/radiologic location
acquisition
setting occur
why do we classify PNA
direct Abx therapy and determine risk of exposure to MDR organisms
PNA epidemiology
2nd mMC cause of hospital acq. infection,
MC in winter months and colder climates
mc in elderly and high mortality rate in very old
PNA pathogenesis
inflammation of lung parenchyma causing filling of the air spaces with exudates, inflammatory cells and fibrin = CONSOLIDATION
host defense mechanisms are defective or overwhelmed
how to organisms enter the lower respiratory tract
inhalation
aspiration
hematogenous spread
classification mechanisms of bacterial mechanisms
community acquired PNA (CAP)
healthcare associated PNA (HCAP)
hospital and ventilator associated PNA (HAP/VAP)
aspiration PNA
CAP
develops outside the hospital or care facility OR
within 48 hrs of admission to hospital
CAP in pts just admitted who has NOT
been hospitalized >2 days in last 90 days
significant healthcare contact (including HD, wound care, chemo, or IV ABX)
has not resided in >14 days in an extended care facility (ECF, SNF)
HCAP
non hospitalized patient or develops before 48hrs of hospitalization in pt with extensive healthcare contact
(IV therapy, HD, wound care, chemo in 30 days, residence in nursing home or long term care facility >14 days, hospitalization 2+ days)
HAP
occurs 48 hours+ after admission and did not appear to be incubating at time of admission
noscicomial PNA
VAP
HAP that develops more than 48-72 hrs following endotracheal ventilation
who is at risk of MDR pathogens?
ABX in preceding 90 days
current hospitalizations (>5 days)
high freq. ABX in community or specific unit
immunsuppressed
presence of risk factors/ family members
CAP bacterial pathogens
typical
Streptococcal app
H. Flu
Moraxella catarrhalis
s. aureus
MAY be anaerobes and gram neg
cause the TYPICAL symptoms of CAP
atypical CAP pathogens
infectious agents that cause “walking PNA”
Mycoplasma pan, legionella, chlamydia pneumo, chlamydophilia psittaci
adult CAP microbiology
bacterial (70-80)
Atypical (10-20)
viral (10-20)
typical pathogens Gram +
strep pneumonia
staph aureus
strep pneumonia
MC bacterial cause of CAP
rates are decreasing due to vaccination
rust colored sputum
staph areus
mc in groups of pt (post-flu, abx tx, HD, IVDA, pulmonary dx_
MRSA CAN cause cavitation
typical pathogens Gram -
H. flu
moraxella catarrali
klebsiella pneumoniae
psuedomonas aeruginosa
gram 0 bacilli
h. flu
cause of PNA in elder and underlying lung dz
routine immunization decreased prevalence
moraxella catarrali
gram - diplococcus
more common in COPD, PCM, neutropenia, and malignancy
often a copathogen
klebsiella pneumoniae
common in COPD, DM, and chronic alcohol abuse
causes necrotizing PNA with jelly sputum
Pseudomonas aeruginosa
only in certain groups of pts :
underlying lung dz repeated courses of Abx DM prolonged glucocorticoids, immunodeficiency recent ventilation
gram negative bacilli
E. coli, enterobacter, serrate, proteus
uncommon
causes severe PNA and req. intensive care unit
atypical CAP organisms
can’t be gram stained or cultured in standard media
mycoplasma species legionella chlamydophila psittaci chlamydophilia pneumoniae chlamydophilia trachomatis
mycoplasma species
atypical
15% of CAP
transmitted by respiratory droplets
legionella
atypical
fresh water (contamination of water systems/aerosols)
two forms of legionella illness
pontiac fever (virus presentation, malaise, fevers HA, benign)
frank PNA (aggressive, high mortality)
chlamydophila psittaci
causes ornithosis
ass. with handling of birds
chlamydophilia pneumoniae
causes mild PNA or bronchitis in teens/young adults
older adults may have more severe, repeated infxn
chlamydophilia trachomatis
STI/PID and cause of PNA in infants and young children
uncommon CAP etiologies
francisella tularensis
coxiella burnetii
francisella tularensis
tularemia or rabbit fever
suspected in hx of rodent exposure
may be bioterrorism
TYPICAL PNA
coxiella burnetii
causes Q fever
suspected in hx of exposure to domestic animals
ATYPICAL presentation
classic CAP presentation
rigors
AMS, hyponatramia, diarrhea, other GI symptoms
rust colored sputum
red jelly sputum
foul smelling sputum
green sputum
exposure to animal vectors
exposure to overcrowded conditions
exposures to contained air or water
suspect what type of PNA:
AMS, hyponatramia, diarrhea, other GI symptoms
legionella
what type of PNA:
rust colored sputum
red jelly sputum
foul smelling sputum
green sputum
rust: pneumococcal
red jelly: klebsiella
green: pseudomonas, haemophilus, pneumococcal
foul smelling: anaerobic
what type of PNA:
exposure to animal vectors
exposure to overcrowded conditions
exposures to contained air or water
birds - C. psittaci
rabbits/rodents - F tularensis, Y pestis
cats, cattle, sheep, goats - C burnetii, B anthracis
crowded conditions: S pneumonia, mycoplasma, chlamydophilia, mycobacterium
water: legionella
clinical picture of atypical PNA
teens and young adults
preceded by pharyngitis or URI
onset is gradual, heralded by HA, malaise, dry cough, GI symptoms, low grade fever, chills
tests in PNA diagnosis
CBC
CXR
blood cultures
sputum gram stain
bacterial factors that facilitate PNA
obstructive lesions COPD tobacco use repeat ABX dysphagia/aspiration periodontal dz
what is considered health care contact?
- IV therapy, HD wound care, chemotherapy (30 days)
- nursing home or long term care facility >14 days
- hospitalization for 2+ days in prior 90 days
why are GN pathogens causing PNA more severe
endotoxins released have high likelihood to cause sepsis or DIC
typical CAP presentation
pt characteristics
65+ with co-morbidities:
COPD/pulmonary dz
DM/CKD
Cardiac DZ
typical CAP presentation
symptoms
accessory muscle use cough (productive/colored) dyspnea pleuritic CP high fever (>101, chills, hypothermia) malaise, anorexia, fatigue
typical CAP presentation
signs and exam findings
tachypnea, tachycardia, decrease bp
dull to percussion, e->a changes
rales or crackles
increased tactile fremitus
wheezing
benefit of hospitalization
observe patient
access to modalities
IV ABX
ensures compliance
drawbacks to hospitalization/alternatives
could get sicker
expensive, time off
alternative would be f/u in 24hrs
more likely to hospitalization if pt:
comorbidities
physical exam findings (HoTN, tacky, AMS, temp)
labs (uncontrolled DM, hypoxia, dehydration)
imaging
CURB-65
Confusion Urea (>20) Respiratory rate (>30 bpm) Blood pressure (HoTN) Age >65
1= outpatient, 2-3 = inpatient, 3+ = ICU
PORT/PSI
more comprehensive scoring system allows risk stratification to determine which pts req. hospitalization
empiric tx of CAP
healthy pt, no ABX exposure
- MACROLIDE (preferred, azithromycin, clarithromycin)
2. Doxycycline
who gets a macrolide in empiric tx of CAP
pts with no comorbidiites and low levels of strep pneumonia resistance
Pack, clarithromycin or doxxy if macrolide allergic
empiric tx of CAP
comorbid/recent ABX
- Respiratory quinolone mono therapy (levoquin, cipro)
2. Beta lactam + macrolide
what doesn’t work for empiric tx of CAP
PCN, E-mycin, TMP-SMX
pneumococcal resistance
how long do PNA pts get ABX
5 days output
die effects of macrolide
QT prolongation
increased LFTs
Warfarin interaction
GI upset
augmentin side effects
GI upset
C Diff risk
PREG SAFE
Fluroquinalones side effects
tendon rupture C diff QT prolongation CNS disturbance CKD dose adjust photosensitivity
telemetry inpatient CAP tx
- B-lactam + macrolide
(ceftriaxone - CKD Ok, Cefotaxime, + Azithro.) - Fluoroquinolone mono therapy
inpatient CAP tx pseudomonas risk
Zosyn
Primaxin
Cefepina
Cetazidime
PLUS fluoro
telemetry inpatient CAP tx
ca-MRSA risk
empiric tx with vancomycin
who to consider severe ca-MRSA
admission to ICU for septic shock/mechanical vent
necrotizing cavitation
Empyemas
GPC clusters on stain
who is at risk for ca-MRSA
ESRD IVDA MSM prisoners recent flu illness, recent ABX
supportive CAP tx
IV hydration, diuretics nutrition pulmonary toiling respiratory tx pain meds supplemental o2 antipyritics
clinical course of pNA
pneumo defervesce in 48-72 hrs
symptoms may take longer (cough 8 days, crackles 3 weeks)
dont change ABX in first 72 hrs
when i sPNA tx refractory to another regimen
TB, viral/fungal PNA
effusion or atelectasis
must do non-contrast CT
when to change ABX from IV to PO
patient is healthy for 24hrs, one dose after that
prevention of CAP
seasonal flu vaccine
pneumococcal vaccine
pneumococcal vaccine
routine use in adults >64 and children 2+ with significant comorbdities
revaccinate in 5 yrs
list the 2 pneumococcal vaccines
conjugate vax (PCV13) - chiffren <5, adults 65+, children >6 with risks
PPSV23- adults 65+, others with risk
Noscocomial PNA
typically caused by
gram negative bacilli aspirated from GI
MAY be S. pneumococcal and S. aureus
pathogenesis of HAP/VAP
colonization of pathogens
aspiration to lower tract
due to immunocompromised its, with direct access to lung (vent, catheters), no coughing
s/s of HAP/VAP
non-specific
fevers (mild), leukocytosis, AMS, new cough, infiltrates on CR
diagnosing HAP/VAP
clinical
easy to collect sputum in ventilated patients but NOT ALL infiltrates are PNA
T or F ALL infiltrates are PNA
FALSE
tx of HAP
mild
3rd gen cephalosporins
beta lactam
respiratory fluoroquinalones
- NO MRSA, Psedomondas cvg
tx of severe HAP/VAP
broad coverage x 7 days
amino glycoside or fluoroquinolone + Zosyn, Cefepime, Carbapenem
fulminant PNA
immunocompromised
secondary to bacterial pathogens
immunocompromised insidious PNA
viral cause
gunwale, protozoan, mycobacteria
management of immunocompromised
aggressive empiric therapy
early invasive testing (bronchoscopy) to consider severe disease and if patients fail to improve
flu presents as
myalgia/malaise, body pain
sudden/abrupt onset of symps
high fever, n/v, dry cough, sore throat
no specific finding
major complication of the flu
development of pneumonia
groups at high risk for flu complications
chronic cardio dz, pulmonary illness
DM, liver, renal dz, immunosuppressed
residents of nursing homes or chronic care
50+
Primary influenza PNA
flu virus directly infects lungs
severe PNA, but rare
primary flu PNA
symptoms
peristent, increasing flu symptoms
high fever
dyspnea
cyanosis
secondary bacterial pneumonia
25% of flu deaths
virus causes epithelium of trachea and bronchioles to decrease size
lose cilia and increase bacterial load = secondary PNA
common secondary PNA pathogens
destruction of bronchioles causes infection
strep pneumo (increased adherence and invasion)
caMRSA
H Flu
clinical presentation
secondary bacterial pneumonia
exacerbation of fever and respiratory symptoms
after initial improvement in symptoms of acute influenza the pt relapses with higher fevers, cough, production of purulent sputum and pulmonary infiltrates
tx of secondary bacterial pneumonia
vancomycin (cMRSA coverage)
leading cause of viral lower respiratory infections in infants
RSV
RSV epidemiology
can be deadly in infants and young children
common in winter, males more likely to be hospitalize
children ages 2-8 months
more severe in those with f/h of asthma, congenital heart dz, chronic lung dz, prematurity and multiple gestations
s/s of RSV
URI symptoms (progresses over 1-2 days) to fever (<101)
cough, wheezing, rales, retractions and cyanosis
secondary infection due to RSV uncommon except AOM
RSV tx
supportive treatment (O2, bronchodilators, and vaporized epinephrine)
RSV prophylaxis
high risk infants
humanized monoclonal anti-RSV Ab during RSV season
fungal PNA
suspected if pt has immunocompromised or PNA
can mimic acute CAP, but also indolent course and cavitation possible
difficult to isolate
common fungal pneumonias
aspergillus
cryptococcus
aspergillus
classical in neutropenic its and on multiple Abx
also common in old pt with COPD on steroids
cryptoccocus
ubiquitous
causes clinically significant dz in immunocomplrimised
less common fungal dzs
histoplasmosis
blastomycosis
coccidomycosis
pneumocystis pneumonia
MC opportunistic infection in HIV
gradual onset over weeks to months
PCP symptoms
fever, non-productive to somewhat productive cough
progressive dyspnea with severe hypoxemia
aspiration PNA
often unseen, common during sleep
may cause acute worsening of asthma, chemical pneumonitis, airway obstruction, pulmonary infection
causes dz in dependent lung zones
who is at risk aspiration PNA
dysphagia (stroke) drugs/alcohol sleep apnea seizures, anesthesia vomiting/GERD
aspiration PNA dz development
quick respiratory distress development, fever, cyanosis, tachypnea/tachycardia, wheezing, hypoxia, and cough, may be productive
liken develop ARDS
aspiration PNA caused by which organisms
staph, strep, anaerobes
esp. in pts swallowing issue, poor hygiene, dysphagia/stroke, alcoholics
aspiration PNA pt presentation
insidious process, presentation present with advanced dz
low grade fever, smelly/productive cough, dyspnea
aspiration PNA tx
must include cvg for CAP, anaerobes
Unasyn, or Augmentin (not severly ill) Clinda can be used x 7 days
pleural effusion = toracentesis
cavitary dz = longer course
complications of PNA
respiratory failure
parapneumonic pleural effusion
empyema
bacteremia
lung abscess
paraneumonic effusions
exudates caused by increased in fluid during PNA
form when resorptive capacity of pleural space
paraneumonic effusions
uncomplicated (stage I)
small, resolves with approtriope ABx
no bacterial in fluid space
lots of fluid may be tx with toracentesis
parapneumonic effusions
complicated
bacterial and neutrophil invasion of pleural space
deposition of fibrin cause location and lung entrapment
tx as if empyema is present (no pus)
empyema
stage III parapneumonic effusions
Pus in pleural space
req. drainage
tx of empyema
complete fluid drainage
sterilization of cavity
adequate lung expansion
lung abscess
necrosis of tissue with fibrous vanity caused by bacterial and fungal infection
indolent course of fever, night sweats weight loss and cough
mc source of lung abscess
complication of aspiration pneumonia (7-14 days later, weeks to frank abscess)
pathophysiology of lung abscess
free. caused by anaerobes from gingiva
mc in its at risk for aspiration - alcoholics pts with poor hygiene, chronic dz bc PERIODONTAL DZ impaired swallowing or pulmonary defense mechanisms
making dx lung abscess
CXR reveals cavitary lung lesion +/- air fluid level
CT scan w/contrast = Study of Choice
other cavitary dzs considered
lung abscess tx
3+ weeks Abx IV
Empiric therapy with Unazyn or carbapenem
Augmentin ok orally
most of time - sx not required
percutaneous abscess draining or resection reserved for its who don’t respond to management
