IC16 LRTI Flashcards
What is acute bronchitis? What is the signs and symptoms of acute bronchitis? How would you treat it? What are the criteria for returning to see the dr?
Acute Bronchitis
Inflammation of the trachea and lower airways
Mostly viral cause
Need differential diagnosis:
- common cold, cold variant asthma, COPD, lung cancer, acute exacerbation of bronchiectasis, acute exacerbation of chronic cough in smoker, acute rhinosinusitis
Diagnosis:
- based on clinical presentation
- NO need diagnostic test
Treatment:
- Self-limiting
- No need antibiotics UNLESS secondary bacterial infection
o then will use antibiotics for that rather than for the acute bronchitis)
Clinical Presentations: Acute Cough for < 3wks (NOT more than 3wks)
Return or call the clinic:
1. Fever
2. Shortness of breath
3. Chest pain
4. Cough increases in extent or frequency
5. Significant cough persists beyond 3 weeks
What are the difference between acute bronchitis and pneumonia:
Points Bronchitis Pneumonia
Cause of infection: Viral_Bacterial (rarely fungal or viral)
Site of infection: trachea and large bronchus_alveoli and lung parenchyma
S&S: Acute cough 3wks or less_A lot (below)
Treatment: Self-limiting. Unless worsens into bacterial infection (need antibiotics)_Antibiotics depending on the type and severity of the pneumonia
What is pneumonia and the pathophysiology?
- Lower respiratory tract infection (LRTI)
- infection and thus inflammation of the alveoli and surrounding lung tissues
- infection of the lung parenchyma
- proliferation of microbial pathogens in the alveolar structure
o Exudate into alveoli –> fluid accumulation –> cough
o Affect gas exchange –> hypoxia –> tachypnea
o inflammation (vasodilation) –> hypotension
What are the source of infection of pneumonia?
- Aspiration of oropharyngeal secretions
- Inhalation of aerosolized droplets
- Hematogenous spreading (bloodstream)
What are the generel risk factors of pneumonia?
- Smoking –> reduce neutrophil function and damage lung epithelium
- Chronic Lung Diseases –> asthma, COPD, lung cancer –> destroy lung tissue and offer more niduses for infection
- Immune Suppression –> HIV, corticosteroids, sepsis, chemotherapy
What are the risk factors of CAP and how to prevent CAP?
- History of Pneumonia
- Smoking, chronic lung diseases, immune suppression
Prevention:
- Smoking cessation
- Immunization (influenza, pneumococcal)
What are the subjective evidence of CAP?
Clinical Presentations of Pneumonia:
Systemic: Fever, chills, malaise, mental status change, tachycardia, hypotension
Local: Cough (dry), chest pain (from coughing), shortness of breath, tachypnea (>24bpm), hypoxia, increased sputum production
Lung auscultation (Physical Examination)
- Diminished breath sounds when inhaling
- Crackling when lung expands
What are the objective evidences for pneumonia?
X-ray for everyone with suspected pneumonia
- Need X-ray (or CT scan or MRI)
a. New infiltrates or consolidation (white patches)
b. Should be unilateral - General Lab test (WBC, CRP, Procalcitonin)
- Urinary Antigen test (for severe CAP or hospitalized pts)
a. test whether patient had exposure to it but doesn’t tell whether it was in the past or now since it can still be positive even after on antibiotics - Gram stain & Culture
a. Sputum
i. Less yield
ii. Contaminated – by oropharyngeal secretions
b. Lower respiratory culture
i. Bronchoalveolar lavage (BAL)
ii. Invasive
iii. Less contaminated
c. Blood culture (for hospitalised pts)
i. Rule out bacteremia
Blood and respiratory gram stain and culture done in hospitals for:
- Severe CAP (use IDSA criteria)
- Risk factors for DRO e.g. MRSA/PA
a. Empirically treated for MRSA/PA
b. Infected with MRSA/PA in the last 1 year
c. Hospitalized / Parenteral antibiotic in the last 90 days
What are CAP, HAP, VAP?
Community-acquired Pneumonia:
1. Onset in community
OR
2. <48hrs after hospital admission
Hospital-acquired Pneumonia:
48hrs or more after hospital admission
Ventilator-associated Pneumonia:
48hrs or more after starting on mechanical ventilation
What do you use to determine how to treat CAP?
CURB-65 and IDSA criteria for severe CAP
What is CURB-65?
Determine where to treat patient
5 variables, 3 mortality risk classes
1. Confusion (new onset)
2. Urea > 7 mmol/L
3. Respiratory rate >= 30 breaths per min
4. Blood Pressure < 90/60mmmHg
5. >= 65 y/o
Classes:
0 and 1 –> Outpatient
2 –> inpatient
3 or more –> inpatient and consider ICU
What is IDSA criteria?
To consider as severe CAP
1 or more major criteria:
- Mechanical ventilation
- Septic shock requiring vasoactive medications
OR
3 or more minor criteria:
- RR >= 30 bpm
- PaO2/FiO2 <= 250
- Urea > 7 mmol/L (uremia)
- Leukopenia (WBC < 4 x 10^9/L)
- Multilobar infiltrates (extensive)
- Confusion / disorientation
- Hypothermia (core temp. < 36 degrees)
- Hypotension requiring aggressive fluid resuscitation
What is the likely pathogen(s) that cause outpatient CAP without comorbidities? What is the empiric therapy?
Outpatient (NO comorbidities)
Pathogen:
1. Streptococcus Pneumonia
Empiric therapy:
1. PO Amoxicillin 1g Q8h
(2nd line: PO levofloxacin / moxifloxacin)
Ciprofloxacin does not cover streptococcus p.
High dose amoxicillin to takckle penicillin resistant strep pneumonia
All 5 days
What is the likely pathogen(s) that cause outpatient CAP with comorbidities? What is the empiric therapy?
Outpatient (WITH comorbidities e.g. chronic heart, lung, liver or renal disease; DM; alcoholism; malignancy; asplenia)
Pathogen:
1. Streptococcus pneumonia
2. Hemophilus influenza
3. Atypicals
Empiric therapy:
1. PO Augmentin / cefuroxime
AND
2. PO Macrolide (clarithromycin / azithromycin) OR doxycycline
(2nd line: PO levofloxacin / moxifloxacin)
Macrolides vs doxycycline:
Look at ADR for atypicals cover
Clarithro vs azithro:
lower CYP3A4, once daily dosing, cheap
Ciprofloxacin does not cover streptococcus p. or atypicals
PO Levofloxacin 750mg OD
What is the likely pathogen(s) that cause inpatient non-severe CAP? What is the empiric therapy?
Inpatient Non-Severe
(IV or oral depending on patient’s ability to swallow)
Pathogen:
- Streptococcus pneumonia
- Hemophilus influenza
- Atypicals
- MRSA
a. MRSA resp isolate in last 1yr
b. Hospitalized / Parenteral antibiotics in the last 90days AND positive MRSA PCR screen - Pseudomonas aeruginosa
a. PA resp. isolate in the last 1yr
Empiric therapy:
- Augmentin / cefuroxime / ceftriaxone
AND - Macrolide (clarithromycin / azithromycin) OR doxycycline
(2nd line: levo / moxifloxacin)
AND
- IV Vancomycin or PO/IV Linezolid
MODIFY (not add on)
- Pip-tazo, cefepime, ceftazidime, meropenem, levofloxacin
5 days
7 days (if have MRSA/PA coverage)
What is the likely pathogen(s) that cause inpatient severe CAP? What is the empiric therapy?
Inpatient Severe (IV)
Pathogen:
- Streptococcus pneumonia
- Staphylococcus Aureus
- Hemophilus influenza
- Atypicals
- MRSA
a. MRSA resp. isolate in last 1yr
b. Hospitalized / Parenteral antibiotics in the last 90 days - Pseudomonas aeruginosa
a. PA resp. isolate in the last 1yr
b. Hospitalization / Parenteral antibiotics in the last 90 days - Other Gram negative e.g. klebsiella pneumonia, burkholderia pseudomallei
Empiric therapy:
- IV Augmentin / Pen G
AND - IV Ceftazidime
AND - IV Macrolide (clarithromycin / azithromycin)
(2nd line: IV levofloxacin / moxifloxacin + ceftazidime)
AND
4. IV Vancomycin or PO/IV Linezolid
Ceftazidime covers burkholderia pseudomallei & pseudomonas aeruginosa
No Doxycycline since no IV form
Pen G + ceftazidime is narrow spectrum
Ceftazidime / levofloxacin would have covered pseudomonas, so no need to modify therapy
5 days or 7 days (if need MRSA/PA coverage)
moxifloxacin can cover bacteroides if anaerobic coverage needed
What other things to take note of when treating CAP?
- If have lung abscess / empyema, reported in radiology investigations, give anaerobe coverage
a. If standard regimen no anaerobe coverage –> give IV/PO metronidazole / IV/PO clindamycin
b. Augmentin + ceftazidime + azithromycin
c. Moxifloxacin + ceftazidime - If suspected to have influenza, check and manage influenza in all patients during peak seasons
a. Add oseltamivir 75mg BD 5days (within 48 hrs, up to 5 days of symptoms onset)
b. If positive culture/influenza PCR, complete oseltamivir course of 5 days
c. If no bacterial pathogen evidence (negative culture, low procalcitonin levels, and early clinical stability), stop antibiotics at 48 to 72 hours - Avoid using respiratory FQ e.g. Levofloxacin / moxifloxacin as 1st line for CAP
a. Lots of ADR
i. Tendinitis, tendon rupture
ii. QTc prolongation
iii. Neuropathy
iv. CNS disturbances
v. Hypoglycemia
vi. Arthropathy
b. Avoid developing resistance against them and other antibiotics
c. Save for serious gram-negative infection
i. When have severe penicillin allergy
ii. Only PO options for pseudomonas aeruginosa
d. Delay diagnosis of tuberculosis
e. Undesirable monotherapy if have tuberculosis - Adjunctive corticosteroids therapy
a. Reduce inflammation in lungs
b. USE if shock refractory (not responding) to fluid resuscitation or vasopressor support
c. NOT use / conflicting evidence in non-severe or severe CAP respectively
d. E.g. PO prednisolone, IV dexamethasone, hydrocortisone
When to deescalate for CAP?
De-escalation:
When:
- Hemodynamically stable (BP normal)
- Clinically improving
- IV to oral – if patient can take oral meds
How:
- Positive Culture:
o Follow AST to change to narrow spectrum or
PO antibiotics - No culture:
o Stop coverage for MRSA, pseudomonas, burkholderia within 48 hours (if pathogen not isolated and patient improving)
o IV to oral –> use either same antibiotics or another antibiotic from the same class (e.g. PO Augmentin + PO clarithromycin)
What is the duration of treatment for CAP?
Duration:
- Minimum 5 days
- 7 days if treating MRSA / pseudomonas
- Longer (2-3wks / 3-6 weeks / 6months)
o Deep-seated infections (e.g. lung abscess, meningitis)
o less common pathogen (e.g. TB, burkholderia pseudomallei, fungi)
How to monitor response?
Step 4: Monitor Response
Therapeutic:
- should improve within 48 to 72 hrs
- elderly / those with comorbidities might take longer time to improve
- Escalation: Do not escalate within the 1st 72 hours –> let antibiotics work
o Unless culture-directed or significant clinical deterioration - Clinical Stability / Improvement:
o resolution of vital sign abnormalities e.g. heart rate (~70bpm), respiratory rate (12-22 bpm), blood pressure (~120/80 mmHg), oxygen saturation (95-100), temperature (>36 degrees)
o ability to ingest oral medications
o baseline mental status - NO need for radiographic repeats e.g. X-ray
o Unless significant clinical deterioration - NO need for lab test e.g. sputum culture, urine culture
Toxicity:
- ADR of antibiotics
What are the risk factors for HAP/VAP and the prevention methods?
Patient related factors:
- Elderly
- Smoking
- COPD, cancer, immunosuppression
- Prolonged hospitalization
- Coma, impaired consciousness (affect swallowing and breathing)
- Malnutrition (reduce immunity)
Infection control-related factors:
- Lack of hand hygiene
- Contaminated respiratory care device e.g. supplement oxygen mask
Healthcare-related factors:
- Prior antibiotics use
- Sedatives
- Opioid analgesics
- Mechanical ventilation
- Supine position
Prevention:
- Practice consistent hand hygiene (infection control)
- Judicious use of antibiotics and medications with sedative effects (health-related)
- VAP specific (healthcare-related)
o Limit duration of mechanical ventilation
o Minimize duration and deep levels of sedation
o Elevate head of bed by 30 degrees
What are the subjective evidences for HAP/VAP?
same as CAP
Clinical Presentations of Pneumonia:
Systemic: Fever, chills, malaise, mental status change, tachycardia, hypotension
Local: Cough (dry), chest pain(from coughing), shortness of breath, tachypnea (>24bpm), hypoxia, increased sputum production
Lung auscultation
- Diminished breath sounds when inhaling
- Crackling when lung expands
What are the objective evidences for HAP/VAP?
- Need X-ray
a. New infiltrates or consolidation (white patches) - General Lab test (WBC, CRP, Procalcitonin)
- Urinary Antigen test (for severe CAP or hospitalized pts)
a. test whether patient had exposure to it but doesn’t tell whether it was in the past or now since it can still be positive even after on antibiotics - Gram stain & Culture
a. Sputum
i. Less yield
ii. Contaminated – by oropharyngeal secretions
b. Respiratory culture
i. Bronchoalveolar lavage (BAL)
ii. Invasive
iii. Less contaminated
c. Blood culture (hospital pts)
i. Rule out bacteremia
Blood and respiratory gram stain and culture done in hospitals for:
Risk factors for DRO e.g. MRSA/PA
- Empirically treated for MRSA/PA
- Infected with MRSA/PA in the last 1 year
- Hospitalized / Parenteral antibiotic in the last 90 days
What to consider when treating/deciding on the therapy for HAP/VAP?
Minimally need coverage for Pseudomonas aeruginosa and staphylococcus aureus
Need additional coverage based on:
- MDRO risk factors
- Mortality risk factors
- Hospital’s / unit’s distribution of pathogen-associated with HAP/VAP and their susceptibilities e.g. antibiogram
Cover for MRSA, if:
- Prior IV antibiotics in the last 90 days
- Isolation of MRSA in last 1 year
- Hospitalization in unit where 20% of S. aureus are MRSA
- High mortality risk e.g. need ventilatory support due to HAP and septic shock
Pseudomonas & GNR – Double antipseudomonal antibiotics from different classes for VAP/HAP empiric treatment:
- Antimicrobial resistance risk factor
a. IV antibiotics use in last 90 days
b. Acute renal replacement therapy (dialysis) prior to VAP onset
c. Isolation of Pseudomonas aeruginosa in last 1 year - Hospitalization in unit with 10% of PA being resistant to monotherapy agent
- High mortality risk e.g. on mechanical ventilator due to HAP and septic shock
- VAP??
AVOID use of aminoglycosides as the sole anti-pseudomonal agent
- Nephrotoxicity
- Patients already hypotensive, low blood flow to the kidneys might increase their risk of AKI –> if given aminoglycoside might worsen this
- Don’t penetrate the lung well + don’t go into lung abscess well
