Transcript Hepatitis C - Morning Report

Pneumonia
By:
Nicole Smidt & Sarah Nainggolan
Types of Pneumonia
1. Community-acquired (CAP)
2. Hospital-acquired (nosocomial) (HAP)
3. Ventilator-associated (VAP)
(CAP) Pathophysiology
-CAP is acquired by the body via an inhalational
or aspirational route.
-Sometimes, CAP can be obtained as a secondary
bacteremia from another part of the body
resulting in pneumonia caused by bacteria
common to other areas of the body.
-CAP tends to affect the elderly,
immunocompromised, and those with
underlying lung conditions (i.e. COPD, chronic
bronchitis).
H&P in a (CAP) patient
• History
– Varying degrees of
fever with acute onset
– Productive cough with
yellow/green sputum
– Pleuritic chest pain
– SOB
• Physical
– Auscultation of rales
over the involved lobe
or segment
– Increased tactile vocal
fremitus, bronchial
breathing, and
egophony (e>a sound)
– Purulent sputum
– Blood-tinged sputum
– Signs of consolidation
Bacterial Pathogens of (CAP)
~85% of CAPs
• Streptococcus pneumoniae
– MCC
• H. influenzae
- COPD
• Moraxella catarrhalis
– MC in patients with chronic bronchitis & COPD
Common Pathogens/Atypical Hosts
-Staph aureus causes CAP in the setting of
postviral influenza.
-Klebsiella pneumoniae causes CAP in chronic
alcoholics. Aspiration pneumonia is typically
caused by multiple pathogens.
-Pseudomonas aeruginosa is a cause of CAP in
patients with cystic fibrosis and bronchiectasis.
Atypical Pathogens of CAP
• Zoonotic
– Chlamydia psittaci
• Psittacosis
• Recent close contact with
birds
– Francisella tularensis
• Tularemia
• Contact with deer or
rabbits or recent bite by a
tick or deer fly
– Coxiella burnetii
• Q fever
• Contact with a cat or
sheep that has given birth
recently
• Non-zoonotic
(~15% of CAPs)
– Legionella
– Elderly, smokers,
immunocompromised
– Mycoplasma
pneumoniae
– Young and healthy
– Chlamydia
pneumoniae
– Young & healthy
Atypical CAP
-Atypical pneumonias commonly present with dry
cough, extrapulmonary involvement, and
patchy interstitial pattern on CXR.
Differential Dx of CAP
-Chronic bronchitis
-Myocardial infarction
-Asthma
-CHF
-Pulmonary edema
-PE
-Acute hypersensitivity reaction
-Bronchogenic carcinoma
Laboratory Studies of CAP
-CBC with differential showing a neutrophilia w/left shift,
electrolytes, elevated BUN/Cr, elevated glucose, abnormal LFTs
-Sputum Gram stain and/or culture (should have <10 squamous
cells/lpf/purulent should have >25 PMNs/lpf)
-2-3 sets of blood cultures (before antibiotics) to detect presence of
bacteria in the blood
-Serum cold agglutinin titers (Mycoplasma)
-Urinalysis
-Serological testing if zoonotic atypical pathogens are suspected
Imaging Studies of CAP
-Chest x-ray
*Repeat chest x-ray within 24 hours if first x-ray shows
negative findings with high clinical suspicion
-Serial chest x-rays to observe for progression or check
for resolution
-Chest CT scan
*If failing to respond to therapy
Community Acquired Pneumonia
(CAP) Treatment
• Decision to hospitalize
1. Pneumonia Severity Index (PSI)


Points given for 20 variables i.e. age, comorbid
conditions, abnormal PE & lab findings
Add up the points; patients are categorized into 5
classes
Total points
Risk Class
% Mortality
Treat as:
No predictors
I
0.1
Outpatient
≤70
II
0.6
Outpatient
71-90
III
2.8
Inpatient, briefly
91-130
IV
8.2
Inpatient
>130
V
29.2
Inpatient
Decision to hospitalize, cont.
2. CURB-65
 Five variables
 C=Confusion
 U=Urea > 7mmol/L
 R=Respiratory rate ≥ 30
 B=BP systolic ≤ 90, diastolic ≤ 60
 Age ≥ 65
 Add up the points, patients are categorized into 3
classes
Decision to hospitalize, cont.
• CURB-65, cont.
Total points
30-day Mortality Risk
Treat as:
0
1.5%
Outpatient
1-2
9.2%
Inpatient
≥3
22%
ICU
• PSI-less practical
• CURB-65-less studies done
CAP Treatment
• Empiric antibiotic treatment
– Outpatient treatment
• Previously healthy or no antibiotics in last 3 months
• Comorbidities or antibiotics in last 3 months
– Inpatient treatment
• Non-ICU patients
• ICU patients
CAP Treatment
Outpatient antibiotics
Guidelines per IDSA and ATS
Previously healthy/no antibiotics in last 3
months
Comorbidities/antibiotics in last 3 months
Clarithromycin 500 mg PO BID, or
Levofloxacin 750 mg PO QD, or
moxifloxacin 400 mg PO QD, or
gemifloxacin 320 mg PO QD, OR
Azithromycin 500 mg PO once, then 250
mg PO QD, or
Amoxicillin 1g TID, or
Amoxicillin/clavulanate 2g BID, or
Doxycycline 100 mg PO BID
Ceftriaxone 1-2g IV QD, cefpodoxime 200
mg PO BID, cefuroxime 500 mg PO BID ,
plus a macrolide
CAP Treatment
Inpatient Antibiotics
Inpatient, non-ICU
Inpatient, ICU
Levofloxacin 750 mg PO or IV QD, or
moxifloxacin 400 mg PO or IV QD, or
gemifloxacin 320 mg PO QD
Cefotaxime 1–2 g IV q8h, or ceftriaxone 2
g IV QD, or ampicillin-sulbactam 2 g IV
q8h plus azithromycin or a
fluoroquinolone *
*PCN-allergic: use resp. fluoroquinolone
and aztreonam 2 g IV q8h
Cefotaxime 1–2 g IV q8h, or ceftriaxone
1–2 g IV QD, or ampicillin 1–2 g IV q4–6h,
or ertapenem 1 g IV qd in selected
patients plus a macrolide (oral
clarithromycin or azithromycin; or IV
azithromycin 1 g once, then 500 mg
QD)**
**PCN-allergic: use resp. fluroquinolones
CAP Treatment
Special Considerations
• Pseudomonas
– piperacillin/tazobactam 4.5 g IV q6h, cefepime 1–2 g IV
q12h, imipenem 500 mg IV q6h, meropenem 1 g IV q8h
plus either ciprofloxacin 400 mg IV q12h or levofloxacin
750 mg IV, or
– piperacillin/tazobactam 4.5 g IV q6h plus amikacin 15
mg/kg qd or tobramycin 1.7 mg/kg qd and azithromycin, or
– piperacillin/tazobactam 4.5 g IV q6h plus an
aminoglycoside plus an antipneumococcal fluoroquinolone
– If PCN-allergic: substitute aztreonam
CAP Treatment
Special Considerations
• Community-Acquired MRSA
– Add linezolid 600 mg IV q12h or vancomycin 1 g IV
q12h
CAP Treatment
• Most patients admitted to the hospital for CAP receive IV
antibiotics
• A switch to oral drugs is appropriate, so long as the
patient can ingest and absorb the drugs, is
hemodynamically stable, and showing clinical
improvement
• Duration: Patients are usually treated for 10-14 days, but
recent studies with fluoroquinolones suggest that a 5-day
course is sufficient for uncomplicated CAP.
CAP
Follow-up
• Fever usually resolves within 2 days, while
leukocytosis may improve within 4 days
• Abnormalities in CXR take 4-12 weeks to clear,
depending on the age of the patient and the
underlying lung disease
• Follow-up CXR can be done 4-6 weeks later
• If recurrence is seen in the same lung segment,
possible neoplasm should be taken into
consideration
CAP
Prognosis
• Depends on age, comorbidities, inpatient/outpatient
• Young patients without comorbidities fully recover in
2 weeks
• Older patients with comorbidities take longer
• Overall mortality rates
– Outpatient: < 1%
– Inpatient: 10%, with about 50% of the deaths directly
attributable to pneumonia
Healthcare-associated Pneumonia
1. Hospital-acquired pneumonia (HAP)
2. Ventilator-associated pneumonia (VAP)
The main difference from CAP: significantly lower
incidence of atypical pathogens, EXCEPT Legionella
Hospital-acquired pneumonia
(HAP)
Defined as pneumonia that occurs more than 48
hours after admission but that was NOT
incubating at the time of admission.
The American Thoracic Society further subdivides
nosocomial pneumonia into early (occurring
within the first 4 days of hospitalization) and
late (occurring after the 5th day of admission)
onset.
HAP Pathophysiology
-HAP is primarily acquired though aspiration of
oropharyngeal secretions into the trachea.
-Although uncommon, hematogenous spread is
also possible.
-HAP is mainly caused by aerobic gram-negative
bacilli of two forms: necrotizing and
nonnecrotizing.
*Necrotizing cause rapid cavitation,
microabscess formation, blood-vessel invasion,
and hemorrhage (i.e. P. aeruginosa).
HAP
-Usually bacterial in nature.
-Common in patients with mechanical
ventilation as intubation and ventilation
support bypass the normal host defense
mechanisms.
-One of the most common diagnoses in the
medical and surgical ICUs.
H&P of HAP
History:
-SOB
-Productive cough
-Fever
Physical:
-Rales on auscultation
over affected area
-Generally NO
consolidation in
nosocomial
pneumonia
HAP Microbiology
-P. aeruginosa
-Klebsiella
-E. coli
-Acinetobacter (common in ICU patients)
-Staph aureus
-Strep pneumoniae
-H. influenzae
Dx of HAP
Laboratory:
-White blood cell
count
-Blood cultures
Imaging Studies:
-Serial chest x-rays to
check for
progression and
resolution
-CT or spiral CT scan
Hospital-acquired Pneumonia
(HAP)
•
•
•
•
•
Main differences from VAP:
– Lower incidence of MDR pathogens (allows more
monotherapy)
– Better host immunity
Anaerobes are more common
Specific therapy aimed at anaerobes is not
indicated, unless aspiration is a concern
Lower risk of antibiotic failure in comparison to VAP
Lower mortality rates than VAP
Ventilator-associated pneumonia
Defined as pneumonia that develops 48 hours or
longer after mechanical ventilation is given via
endotracheal tube or tracheostomy.
VAP Pathophysiology
-VAP is caused by invasion of the lower
respiratory tract and lung tissue by
microorganisms caused by decreased integrity
of the oropharynx and trachea allowing oral
and gastric sections to enter.
-The incidence of VAP increases with the duration
of ventilation.
-Pseudomonas and Acinetobacter pneumonia is
associated with the greatest mortality.
Dx of VAP
History:
1. Hospitalization of greater than
5 days
2. Hospital admission of more
than 2 days in the last 90 days
3. Antibiotic use in the last 90
days
4. Residing in a nursing home or
skilled care facility
5. Home infusion therapy or
wound care
6. Dialysis within the last 30 days
7. Immunocompromised
Diagnostic Triad:
1. Fever
2. Purulent secretions
3. Leukocytosis
Work-up of VAP
-CBC with differential to evaluate white blood cell
count
-Routine blood tests to assess patient's baseline
renal and hepatic function to properly dose
antibiotics
-Blood cultures
-Respiratory secretion cultures
-Portable chest radiography
-Air bronchogram
Ventilator-associated Pneumonia
(VAP)
• Empirical Antibiotic Treatment
Patients with NO risk factors for MDR
pathogens
Patients with risk factors for MDR
pathogens
Ceftriaxone 2 g IV q24h, or
1. Ceftazidime 2 g IV q8h or cefepime 2 g IV
q8–12h, or
Moxifloxacin 400 mg IV q24h, ciprofloxacin
400 mg IV q8h, or levofloxacin 750 mg IV
q24h, or
Piperacillin/tazobactam 4.5 g IV q6h,
imipenem 500 mg IV q6h or 1 g IV q8h, or
meropenem 1 g IV q8h, plus
Ampicillin/sulbactam 3 g IV q6h, or
2. Gentamicin or tobramycin 7 mg/kg IV
q24h or amikacin 20 mg/kg IV q24h or
Ciprofloxacin 400 mg IV q8h or levofloxacin
750 mg IV q24h, plus
Ertapenem 1 g IV q24h
3. Linezolid 600 mg IV q12h or
Vancomycin 15 mg/kg, up to 1 g IV, q12h
VAP Treatment
• Duration: 8 days (associated with less
frequent emergence of antibiotic-resistant
strains)
• Pseudomonas aeruginosa: causes high rates
of clinical failure and death, despite combo
therapy
• VAP caused by MRSA: 40% clinical failure rate
when treated with standard-dose
vancomycin, so treat with linezolid instead.
VAP
Follow-up
• Clinical improvement is usually seen within 4872 hours following initial antibiotic therapy
• CXR worsens during initial treatment, so less
helpful
• In very ill patients, follow-up CXR can be done
every few days
• Once patient has improved, CXR may not be
necessary for a few weeks
VAP
Prognosis
•
•
Associated with high crude mortality rates (50-70%)
Stenotrophomonas maltophilia: prognosis is very
poor (death is almost inevitable)
Question #1
From USMLEWORLD
•
A 65-year-old white male who has a history of COPD, CHF, and CAD
presented with a three-day history of worsening SOB, cough with
yellowish expectoration, and fever. He is not on steroids and does not
use oxygen at home. He takes ipratropium, albuterol, aspirin, digoxin,
furosemide, metoprolol, and lisinopril. He lives at home with his wife. His
temp is 103 F, BP is 110/70, pulse is 110, and respirations are 24. He is
saturating 88% on room air. He was started on 3-liters of oxygen to keep
the saturations above 92%. The CXR of the patient is shown below. What
is the most appropriate next step in the management of this patient?
A. Admit the patient and give ampicillin
B. Outpatient trimethoprim-sulfamethoxazole
C. Admit the patient and start levofloxacin
D. Admit the patient and start ciprofloxacin
E. Admit the patient and start vancomycin
F. Outpatient clindamycin therapy
Question #1
CXR
Answer #1
•
C. Admit the patient and start levofloxacin
–
The clinical presentation and CXR of this patient is highly suggestive of CAP.
The first step in the management of CAP is to decide whether the patient
needs hospitalization. The decision to admit the patient is generally made
using the Pneumonia Severity Index (PSI) based on medical history, PE, and
lab and radiographic findings. This patient has other comorbidities such as
CHF, COPD, and CAD, and his oxygen saturation is less than 90%. Thus he
falls under risk class III or IV and needs to be hospitalized.
–
The most common cause of lobar pneumonia in this setting is
pneumococcus. The new generation flouroquinolones (i.e. levofloxacin) is
used for the inpatient treatment of CAP. About 97% of the Streptococcus
pneumonia are sensitive to these drugs. They also cover the atypical
organisms.
–
For the management of outpatient therapy in stable patients with no
comorbidities, either azithromycin or doxycycline can be used.
Question #2
A 68-year-old woman with polymyositis is evaluated in the office because of increased difficulty
swallowing and a 2-week history of low-grade fever, intermittent cough, and sputum production.
On physical examination, temperature is 37.9 °C (100.2 °F), and crackles are heard at the base of
the right lung posteriorly. The leukocyte count is 9700/μL with 85% neutrophils, 12% lymphocytes,
2% monocytes, and 1% eosinophils.
A chest radiograph shows patchy pulmonary infiltrates in the right lower lobe. Sputum Gram stain
shows many neutrophils, a few squamous epithelial cells, and several morphologic types of both
gram-negative rods and gram-positive cocci. Results of sputum culture are pending.
Which of the following is the most appropriate management at this time?
A. Bronchoscopy
B. Clindamycin
C. Metronidazole
D. Penicillin
Answer #2
B. This patient should be started on clindamycin. The presence of underlying polymyositis and difficulty
swallowing place this patient at risk for aspiration and the development of aspiration pneumonia. Other risk
factors for aspiration pneumonia include episodes of depressed consciousness (e.g., patients with alcoholism) or
mechanical factors that increase the likelihood of secretions entering the tracheobronchial tree (e.g., patients
with esophageal obstruction). Although aspiration of acidic gastric contents can result in a chemical
pneumonitis, aspiration of oral secretions typically results in an anaerobic pneumonia caused by anaerobic
organisms that are normally present in the mouth. A sputum Gram stain often shows both gram-positive and
gram-negative organisms of different morphologic types, as was found in this patient. The typical location of
aspiration pneumonia depends upon the patient's position at the time of aspiration. Based on gravitational flow
of airway secretions, the pneumonia is preferentially localized in the dependent regions of the lung at the time
of aspiration. In an upright patient, the lower lobes are usually affected, more so on the right than on the left. In
a supine patient, common sites of aspiration pneumonia are the posterior segment of the right upper lobe and
the superior segment of the right lower lobe.
Although options for antibiotic coverage of anaerobic aspiration pneumonia have generally included either
penicillin or clindamycin, controlled studies have shown that antibiotic failure rates have been higher for
penicillin than for clindamycin. Metronidazole does not adequately cover microaerophilic and aerobic
streptococci from the mouth, which are contributing organisms in many patients with aspiration pneumonia.
Bronchoscopy is not indicated because it is unable to confirm anaerobic infection, since anaerobic organisms
from the mouth will contaminate the specimens obtained.
References
• Mandell LA, Wunderick R, et al. Harrison’s Principles
of Internal Medicine, 17th ed. 2008.
• Chesnutt MS, Gifford AH, Prendergast TJ. Current
Medical Diagnosis & Treatment 2010.
• Agabegi SS, Agabegi ED. Step-Up to Medicine, 2nd
ed. 2008.
• Fischer C, Reichert S. USMLE Master the Boards.
2009.
• Burke A Cunha, MD. Emedicine.medscape.com.
2010.