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1
Q

Asthma Definition

A

-bronchoconstriction, airway wall thickening, increased mucus and variable expiratory airflow limitation.

Asthma Diagnosis requires both:
1. History of variable respiratory symptoms (e.g. wheeze, SOB, chest
tightness, cough) that vary over time and intensity
2. Confirmed variable expiratory airflow limitation:
NEED SPIROMETRY TO HAVE DIAGNOSIS OF ASTHMA

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2
Q

Asthma Phenotypes

A

– Allergic: Classic asthma, atopy, eosinophilic inflammation, responds to ICS
– Non-allergic: Neutrophilic, eosinophilic or paucigranulocytic inflammation with less response to ICS
– Adult-onset: Non-allergic, require higher ICS, rule out occupational asthma
– Associated with obesity: Little eosinophilic inflammation
– Associated with persistent airflow limitation: Longstanding asthma causing
fixed obstruction due to airway remodelling

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3
Q

Asthma Diagnosis

A

Expiratory airflow limitation:
* At least once during diagnostic process, confirm reduced FEV1/FVC (below lower limit of normal)

Variability, as demonstrated by any of:
* Positive bronchodilator reversibility (10-15 minutes after 200-400 mcg salbutamol)
– Improvement in FEV1 by > 12% AND 200mL post BD
* Improvement in lung function with anti-inflammatory treatment x 4 weeks:
– Improvement in FEV1 by > 12% AND 200mL post BD

  • Excessive FEV1 variation in lung function between visits (>12% and 200 cc variation)
  • Peak Flow Variability – Average daily diurnal PEF variability >10%
    – Excessive variability in twice daily PEF over 2 weeks
  • Positive Bronchial Challenge Test or Exercise challenge test (i.e. methacholine challenge, see next
    slides)
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4
Q

Asthma Diagnosis Continued

A

the dose of methacholine that causes a 20% fall in FEV1

  • Airflow limitation may not be present at the time of initial assessment (ie
    can have normal spirometry and still have asthma)
    – If normal, may repeat during times of symptoms
    – Can perform methacholine or exercise testing
  • Methacholine Challenge – look for drop in FEV1 by 20%
    – PC20 <4mg/mL = POSITIVE
    – PC20 4-16 = borderline
    – PC20 >16 = negative
  • Exercise Challenge (Exercise induced bronchoconstriction)
    – Fall in FEV1 of >10% and >200mL from baseline
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5
Q

Assessing Asthma Control

A

The goal of asthma management is asthma control, (includes both asthma symptoms and
risk of future adverse outcomes), asthma control should be assessed at each visit.

Daytime symptoms ≤ 2 d/week

Nighttime symptoms < 1d/ week and mild

Physical activity Normal

Exacerbations Mild (not requiring systemic steroids or ED visit) and infrequent

Absence from work/school due to exacerbation= None

Need for a reliever (SABA or bud/fom) ≤ 2 doses per week

FEV1 or PEF ≥ 90% of personal best

PEF diurnal variation <10-15%

Sputum eosinophils <2-3%

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6
Q

Asthma Basic Treatment Approach

A

2 Do they have risk of severe exacerbation (see Box 1).

CTS 2021 Approach:
#1 Do they have well controlled asthma?
Most new diagnosis of asthma – not well controlled.
IF YES - Go to #2 below
IF NO - start daily ICS + PRN SABA

IF YES - daily ICS (preferred) or PRN bud/form
IF NO -prn Bud/form or PRN SABA*

BOTTOM LINE: Pts should be on daily ICS if they have poorly controlled asthma, or if they have well
controlled asthma but risk for severe exacerbation.

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7
Q

Risk Factors for Severe Exacerbation

A

BOX 1: Risk for severe exacerbation = any 1 of:
* Any history of a previous severe asthma
exacerbation (any of: requiring systemic
steroids, ED visit or hospitalization)
* Poorly controlled asthma per CTS criteria
* Overuse of SABA (=use of more than 2 SABA
inhalers per year)
* Current smoker

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8
Q

Asthma Treatment – LTRA

A

LTRA: may be appropriate as initial controller unwilling/
intolerant of ICS, but less effective than ICS at preventing
exacerbations (GINA)
– Most effective in aspirin-exacerbated asthma, exercise-induced
symptoms, allergic rhinitis
– FDA Black Box Warning: increased suicidality in adolescents and adults

For Adults >12y not achieving asthma control on maintenance
low dose ICS (CTS):
* LABA-ICS is superior to ICS-LTRA
* ↓Exacerbations and Symptoms, ↑QOL and ↑PFT

(Montelukast and zafirlukast)

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9
Q

Uncontrolled vs Severe Asthma

A

SEVERE ASTHMA
Asthma requiring high dose ICS + 2nd
controller for the previous year
* Oral steroids for 50% of the year to
maintain control (or remaining
uncontrolled)

Send additional workup, consider
additional agents on next slide

UNCONTROLLED ASTHMA

  • Poor symptom control
  • Frequent, severe exacerbations ≥
    2/year requiring oral steroids
  • One serious exacerbation requiring
    hospital/ICU/MV in past year
  • Sustained airflow reduction (FEV
    <80% personal best)

Usually due to poor adherence, poor
technique, or ongoing trigger

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10
Q

Severe Asthma Management

A

WORKUP :
* Total IgE
* Peripheral eosinophil count
– Eosinophils >0.3 – consider non-asthma causes including strongyloides serology before systemic steroids [GINA 2023]
– Eosinophils >1.5 – consider investigate for conditions such as EGPA [GINA 2023]
* Sputum eosinophils and FeNO where available
* Consider screening for adrenal insufficiency if pt on maintenance oral corticosteroid or high dose ICS-LABA [GINA 2022]

TREATMENT (akin to STEP 5 on GINA algorithm):
* LAMA / tiotropium mist inhaler for uncontrolled asthma despite ICS/LABA
– Increases time to first severe exacerbation (NEJM 2012)
– Pts should be on at least medium dose ICS/LABA before considering add on
* Macrolides for uncontrolled asthma despite ICS/LABA
– “In individuals >18 w severe asthma there is limited evidence that chronic use of macrolides may
decrease frequency of exacerbations” (LANCET AMAZES Trial 2017)
* Biologics (see next slide) just know they exist
* Low dose oral corticosteroids
* Bronchial thermoplasty: role remains unclear, only to be practiced in specialized centers

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11
Q

Biologics for Severe Asthma

A
  1. Anti-IgE (Omalizumab)
    -Indications: allergic asthma IgE 30 – 700, sensitive to at least 1
    perennial allergen, severe despite high dose ICS and one other
    controller (CTS 2017)
  2. IL-5 (mepolizumab, resilzumab, benralizumab)

-Indication severe eosinophilic asthma (generally >300) and recurrent exacerbation despite high-
dose ICS and one other controller (CTS 2017)

  1. IL-4/IL-13 (Dupilumab) – add-on option for severe eosinophilic asthma or those with nasal
    polyposis or moderate-severe atopic dermatitis.
  2. Anti TSLP (Tezepulumab sc) – add on for severe asthma (including non-allergic). TSLP is a
    cytokine.
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12
Q

Special Populations Asthma

A

Seasonal allergic asthma: start ICS immediately when symptoms
commence, and continue for four weeks after relevant pollen season
ends

  • Exercise induced: salbutamol pre-exercise, if insufficient then LTRA
    pre-exercise, if still insufficient try regular ICS
  • Pregnancy: rule of thirds (1/3 better, 1/3 worse, 1/3 same),
    exacerbations more common, increased risk of preeclampsia, preterm,
    low birth weight, treat as you would anyone else, do not stop ICS, most
    evidence for budesonide of all ICS (though likely all safe), do not
    withhold oral steroids if exacerbating
  • ASA exacerbated respiratory disease (Samter’s triad: asthma, nasal
    polyps, ASA/NSAID sensitivity): avoid ASA/NSAIDs, can treat like
    normal but usually good response to LTRA, desensitize to ASA if
    needed
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13
Q

Asthma ‘Plus’ Syndromes / Asthma mimics

A

Bronchiectasis including Cystic Fibrosis (see Bronchiectasis Section below)

  • Eosinophilic granulomatosis with polyangiitis (EGPA/Churg Strauss)
    – Asthma, eosinophilia, granulomatous vasculitis (cardiac, sinusitis, allergic
    rhinitis, transient pulmonary infiltrates, purpura, neurologic, GI), 30-60% have positive p-anca
    – Treatment: prednisone, cyclophosphamide if severe disease
  • Vocal cord dysfunction
    – Abrupt onset inspiratory stridor, may be misdiagnosed as asthma or
    complicate asthma
    – Dx via laryngoscopy with adduction of the vocal cords upon inspiration
    – Rx: education, behavior modification, speech therapy, treat GERD
  • ABPA
    – Exclusively seen in either asthma or CF
    – Have recurrent exacerbations, fever, brown sputum
    with ‘casts’
    – Criteria: ARTEPICS
    – Treatment: prednisone +/- itraconazole
  • Exercise induced bronchoconstriction

(exercise induced asthma)

– Asthma that develops only during activity
– Should be confirmed with objective testing – fall in
FEV1 >10%, 200mL
– Prn SABA acceptable in this population

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14
Q

Work Related Asthma

A

Occupational asthma: asthma caused by exposure to irritants at
work:

  • Sensitizer-induced asthma (typically long-term exposure)
  • Irritant-induced asthma (RADS=Reactive airways dysfunction syndrome) – one specific high-level exposure

Acute form of irritant induced (often occupational) asthma with symptoms
promptly following a single high dose exposure to vapors, gas or fumes (ie
chlorine, bleach), lasts > 3 months, treat like asthma exacerbation

  • Work exacerbated asthma – pre-existing asthma worse at work
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15
Q

Management of Asthma Exacerbation (GINA)

A

Self-management: written asthma action plan
– May include increased anti-inflammatory reliever
– May include prescription for OCS. Instructions on when to commence
* Primary care: Severe or life-threatening: transfer to acute care
– Pillars: rapid-acting bronchodilators (salbutamol), systemic corticosteroids,
oxygen supplementation
– Antibiotics not recommended.
* ED or Acute Care: Life-threatening: consult ICU, prepare to intubate
– SABA, Atrovent, Oxygen, Steroids
– Consider IV magnesium, high dose ICS
– Avoid sedation. Theophylline and antibiotics not recommended

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16
Q

COPD- Diagnosis

A

Diagnosis: Spirometry is required to make the diagnosis, with a post-bronchodilator FEV1/FVC<0.70

Severity of Airflow Limitation in COPD:
In pts w/ post-bronchodilator FEV1/FVC <0.70:
* Mild: FEV1 > 80% predicted
* Moderate: 50% < FEV1 < 80% predicted
* Severe 30% < FEV1 < 50% predicted
* Very Severe: FEV1 < 30% predicted

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17
Q

COPD Phenotypes

A

Proposed “Etiotypes” in 2023 GOLD guidelines

COPD-P (from pollution exposure) in those exposed to smoke or biomass fuel
COPD-A: COPD and asthma (particularly childhood asthma)
COPD-G : Genetic (AAT)
COPD-C : Cigarettes / Due to smoking
COPD-I : Infection / due to infections (eg Tb, HIV)

Test those diagnosed with COPD for
alpha-1 antitrypsin ONCE

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18
Q

COPD Assessment

A

Determine disease severity: Airflow limitation via FEV1
* Impact on patients’ health status: mMRC and/or CAT (COPD Assessment Test) scores
* Labs: Alpha Anti Trypsin ONCE for all
* Imaging: GOLD 2023 - CT thorax if
* Lung Cancer screening criteria (see med onc lecture)
* Frequent exacerbations (rule out bronchiectasis or atypical infection), symptoms out of proportion of
lung fxn testing
* Lung volume reduction surgery might be helpful (FEV1 <45% and significant gas trapping)
* Assess Risk of future events: Exacerbations, hospitalizations, death

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19
Q

Non-Pharm treatments with SURVIVAL benefit

A

Non Pharmacologic Therapy
– Smoking Cessation: increased survival for all, decreased rate of decline of FEV1

– Long term Oxygen Therapy: increased survival in severe resting hypoxemia
* Should be offered to patients with severe hypoxemia (PaO2<55 mmHg), or when PaO2<60
mmHg in the presence of bilateral ankle edema, cor pulmonale or Hct >56% (CTS guidelines)

-No benefit in moderate resting or exercise-induced moderate desaturation

– Pulmonary Rehabilitation (CTS 2010 Pulmonary Rehab Guideline)
*Pulmonary rehab ↑ exercise capacity, symptoms, QOL across all grades of COPD (GOLD 2022)
* ↓exacerbations if started following RECENT (<4 week) AECOPD
* Increased survival compared with usual care <4 week post AECOPD

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20
Q

COPD Management:

A

Treatment is based on subjective level of dyspnea and rate of exacerbations, NOT lung
function. High risk for AECOPD is defined as 2 or more exacerbations in the past year or 1 or more requiring hospitalization.

-see MMRC dyspnea scale

LAMA or LABA Monotherapy- symptom burden -LOW
(CAT <10, mMRC≤1) , FEV1≥ 80

LAMA/LABA Dual
Symptom burden MODERATE (CAT≥10, mMRC≥2) FEV1 < 80

LAMA/LABA/ICS Symptom burdern MODERATE to HIGH
(CAT≥10, mMRC≥2), FEV1 < 80, + high risk of AECOPD

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21
Q

COPD Rx to Prevent Acute Exacerbations

A
  • Recommended (= Gr1, definitely reduces exacerbations)
    – Annual flu vaccine
    – Pulm Rehab (if RECENT exacerbation <4 weeks ago)
    – Education and Case Management
    – Inhaled pharmacotherapy :as per previous slides
  • Suggested (“consider these” – mixed evidence of reduced exacerbations, but logically they
    will help COPD patients, Gr2C recommendation CTS 2017)
    – Pneumococcal vaccination
  • Since CTS 2017 there’s a good Cochrane Review demonstrating NNT=8 for pneumococcal
    vaccination to prevent AECOPD (and reduces CAP in pts w COPD), so practically recommend to
    all! (Walters JA et al, 2017)

– Smoking Cessation [this reduces mortality and CV events. This is exam MCQ fodder,
practically ask everyone to stop smoking]

  • Do not use the following to prevent AECOPD
    – Systemic corticosteroids >30d after initial exacerbation, theophylline
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22
Q

COPD Management - beyond Inhalers

A

Macrolide Symptom burden MOD to HIGH
CAT≥10, mMRC≥2), high risk AECOPD
FEV1 <80

Roflumilast (PDE-4 inhibitor) or N-acetylcysteine (MUCOLYTIC , antioxidant) for chronic bronchitis phenotype. MOD to HIGH disease burden CAT≥10, mMRC≥2), FEV1 <80

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23
Q

Dyspnea in Advanced COPD (CTS 2011)- Recommendations

A

– oral (but not nebulized) opioids
(Grade 2C)
– neuromuscular electrical muscle
stimulation (Grade 2B)
– chest wall vibration (Grade 2B)
– walking aids (Grade 2B)
– pursed-lip breathing (Gr 2B)
– continuous oxygen therapy for
hypoxemic COPD patients reduces
mortality, and may reduce dyspnea
(Grade 2B)

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24
Q

Asthma-COPD overlap ACO- Diagnosis

A

Asthma-COPD overlap characterized by persistent airflow limitation with
several features of both asthma and COPD
– Worse outcomes than COPD or asthma alone
* ↑ exacerbation, ↓ QOL, ↓ lung function
* ↑ mortality

– REQUIRED:
1. Diagnosis of COPD given risk factors, history, spirometry
2. History of asthma (past history/diagnosis, current symptoms consistent, or
physiology confirmed /w spirometry)
3. Spirometry: post-bronchodilator fixed FEV1/FVC <0.7
– Supportive but not required:
1. Documentation of a bronchodilator improvement of FEV1 by 200ml or 12%
2. Sputum eosinophils >3%
3. Blood eosinophils >300 cells/uL (current or prev documented)

TX:

– Per GOLD: treat as asthma.
– LABA-ICS combo first line
– For refractory symptoms, add LAMA to LABA-ICS combo
– Caveat there are no RCTs addressing this population (asthma trials exclude
smokers, COPD trials exclude asthmatics)

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25
Q

Advanced Therapies

A

NIV in Stable COPD with Hypercapnia
– CTS 2022: Suggest chronic NIV for patients with severe COPD on home oxygen and chronic hypercapnia
(PaCO2 ≥52)
– Several trials showing reduction in hospital re-admission rates; some showing mortality benefit

Lung Volume Reduction Surgery:
– Surgical procedure in which parts of the lung are resected to reduce hyperinflation improving the
effectiveness of the respiratory muscles
– Increased survival in severe emphysema patients with upper-lobe predominant disease and low
post-rehabilitation exercise capacity (NETT trial 2003)
– Bullectomy may be considered in select patients with large bulla

Lung transplant:
– Bode score 7-10 and 1 of 1) hospitalized with COPDE with pCO2 >50 2) pulmonary hypertension/cor
pulmonale despite supp oxygen 3) FEV1 <20% with DLCO <20%
– Shown to improve QOL and functional capacity

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26
Q

AECOPD - diagnosis and treatment

A

Treatment:
– Supplemental oxygen
– Short-acting BD with long-acting BD initiated ASAP prior to discharge
– Steroids x 5-7 days – Shorten recovery and hospitalization duration
– Antibiotics x 5-7d (when indicated) – Shorten recovery, reduce relapse/treatment
failure
– NIV

Antibiotics should be given in COPD in the presence of three cardinal symptoms (or
two of the following if increased purulence* is one of them) or if patient requires
ventilation (NIV or invasive):
1. Increase in dyspnea
2. Increase in sputum volume
3. Increase in sputum purulence

  • Length: 5-7 days [Recommend ≤ 5d if outpt based upon meta-analysis]
  • Choice of antibiotic based on local resistance pattern. Usual choice includes amox-
    clav, macrolide, tetracycline or in selected pts, a resp FQ.

BiPAP/NIV
– AECOPD: Preferred over invasive ventilation if no contraindication
– Significant mortality benefit and reduction in intubation rate
– Recommended (GOLD 2023) if any of:
* pH ≤7.35 with paC02 ≥ 45
* severe dyspnea (impending respiratory failure)
* persistent hypoxemia despite supplemental oxygen

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27
Q

Bronchiectasis

A

“Bronchiectasis is a chronic respiratory disease characterized by a clinical syndrome of cough, sputum
production and bronchial infection, and radiologically by abnormal and permanent dilatation of the
bronchi.
* Most common symptoms:
– Cough with sputum and/or hemoptysis
– Dyspnea and fatigue
– Rhinosinusitis
– Thoracic pain

Work up should be directed based on history and physical. Everyone should get chest CT and PFTs (expect
obstruction). Most common causes are post-infectious and idiopathic (accounting for 50% of cases)

28
Q

Bronchiectasis Work-up

A
  • Allergic BronchoPulmonary Aspergillosis (ABPA):
    – Blood count
    – Total IgE
    – Sensitization to aspergillus (IgE-specific antibodies or skin prick)
  • Serum immunoglobulins (IgG, IgA, IgM)
  • Test for CF (sweat test) and Primary Ciliary Dyskinesia (nasal nitric oxide)
  • Sputum cultures
  • Consider:
    – RF, anti-CCP, ANA, ANCA
    – Alpha1 anti-trypsin
    – Videofluoroscopic swallow study
    – HIV testing
29
Q

Bronchiectasis Treatment

A

Mainstays of treatment:
* Airway clearance: Active cycle of breathing technique
* Mucoactive agents: Hypertonic saline (avoid DNAse unless CF!)

  • Antimicrobials - Inhaled colistin or gentamicin (if Pseudomonas (PsA) colonized)
  • Chronic azithromycin if recurrent exacerbations (with or without PsA colonization but rule out NTM)
  • Bronchodilator: Unless otherwise indicated, may offer as trial if significant breathlessness
  • Pulmonary rehab: If functionally limited by dyspnea (mMRC ≥1)
  • Vaccines: Influenza, Pneumococcal, (+ TdAP, COVID, etc per NACI guidelines)
  • Supplemental oxygen (same criteria as for COPD)
  • Do not routinely offer ICS, oral steroid, PDE4-I
30
Q

Bronchiectasis Advanced Treatment

A

Advanced Therapies:
- Consider surgery / lung resection in localized disease
- Consider transplant if poor lung function and one of: massive hemoptysis, severe PH, ICU admissions or
respiratory failure (require NIV)
- Consider NIV if respiratory failure with hypercapnia, especially if recurrent hospitalization

31
Q

Bronchiectasis Exacerbation

A
  • Obtain sputum cultures
  • Empiric antimicrobials, covering organisms previously grown, if known*
    *no evidence to show antibiotics guided by sensitivity results improves outcomes
  • Generally 14 day course recommended, especially if PsA colonized
    – Shorter course possible if mild bronchiectasis
  • Consider IV antimicrobials if unwell/admitted, resistant organisms or failed
    oral therapy

Major Hemoptysis
– IV antimicrobials
– Tranexamic acid
– Consider embolization as first line

32
Q

Interstitial Lung Disease- Approach

A

History/ Physical
* Family History
* Drugs and radiation
* Inorganic exposures
o asbestos, mining,
sandblasting, etc
* Organic exposures
o mould/water damage,
birds, farms, feather
pillows, hot tubs, etc
* Connective tissue disease
o joints, rash, mechanics hands,
Gottrens, Raynaud’s Shawl
sign, heliotrope, scleroderma
findings, proximal muscle
weakness, etc)

Investigations
* ALL: ANA, RF, anti- CCP
* send more serology if
clinically indicated
* HRCT Chest
* PFTs +/- 6MWT +/- home ox
assessment
* Can send precipitating antibodies
for some known antigens for HP
* Respirology +/- Rheumatology
Referral
* Sometimes lung biopsy

33
Q

Idiopathic Pulmonary Fibrosis (IPF)
-Diagnosis Requirements

A

Most common IIP
* M > F, 6th or 7th decade (rare <50)
* Many have smoking history
* Chronic, progressive, fibrotic ILD defined by the histologic and/or
radiographic pattern of Usual Interstitial Pneumonia (UIP)

  • Diagnosis requires:
    1. Exclusion of other known causes of ILD
    2. Demonstration of UIP pattern on high-resolution CT (see next page)
    3. Specific combinations of HRCT pattern and histopathology patterns in patients subject to tissue biopsy (most do not require biopsy)
    + Consensus of Specialist after Multidisciplinary Discussion (MDD)
34
Q

Radiology of IPF (UIP pattern)

A
  1. Reticular Changes
  2. Subpleural/Basal predominant
  3. Honeycombing
  4. Absence of inconsistent features

Predominant Distribution:
* Peribronchovascular
* Perilymphatic
* Upper or mid-lung

  • Assess for environmental and medication exposures to rule out
    other causes of ILD
  • Send serologic testing: ANA, RF, anti-CCP +/- myositis panel +/- Rheum referral
  • Referral to Respirology: Patients with new diagnosis of suspected
    IPF should undergo Multidisciplinary Discussion (MDD)
  • Consideration for further diagnostics (bronchoscopy and BAL,
    transbronchial lung cryobiopsy or surgical lung biopsy, etc.) will
    be the decision of the MDD
35
Q

IPF Treatment

A
  • Quit smoking, oxygen therapy, pulmonary rehab, Pneumovax and influenza
    vaccination (+ COVID, + update TdaP per NACI…)
  • Do not give PPI for purpose of improving resp outcomes (just Rx if indicated for usual
    GI reasons) – ATS 2022
  • Anti-fibrotic medications (both reduce decline in FVC by about 50%):
    – Nintendanib (INPULSIS 1/2 trials) – TK inhibitor, resulted in reduced FVC decline, pooled
    analysis shows trend to reduced mortality. Adverse effects: diarrhea, GI upset, transaminitis
    – Pirfenidone (ASCEND/CAPACITY trials) – reduced FVC decline, 6MWTD decline, pooled analysis
    showed improved survival.
  • No role for corticosteroids or immunosuppression in IPF given increased mortality
    (PANTHER-IPF) !
    Acute exacerbation:
    – Worsening dyspnea, hypoxemia with new diffuse bilateral ground glass on CT
    – Rule out infection/PE/HF
    – Consider high dose corticosteroids (1g/d x 3 -> 1mg/kg po daily) and empiric antimicrobials
    – Dismal prognosis – generally 50% in-hospital mortality
36
Q

Anti-Fibrotics in Non-IPF ILD

A

ATS 2022 IPF : conditionally “suggest nintedanib for treatment of
progressive pulmonary fibrosis (Non IPF) in patients who have failed
standard therapy for ILD”
– Caveats ++ More research needed

37
Q

Pleural Effusion-When to do a thoracentesis

A

When to do a thoracentesis
– Aspiration should NOT be performed for bilateral effusions in a clinical setting strongly suggestive of a transudate / heart failure

– Thoracentesis should be considered if:
* Suspect exudate
* Cause unclear
* Parapneumonic effusion (as per CHEST guidelines, if less than 1 cm of fluid on lateral decubitus in context of pneumonia can forgo
sampling and instead follow radiographically)
– Image guidance (US) should be used to reduce risk of complications (BTS 2023)

38
Q

How to investigate exudate NYD?

A

Exudate NYD:
* Can repeat thoracentesis once for increased sensitivity;
sensitivity of pleural fluid cytology for malignancy
increases to approx 80% with two thoras
* At least 25cc, preferrable 50cc
* Get CT chest
* Refer for pleural biopsy: Can do CT guided if area of
obvious abnormality
* Thorascopy with pleural biopsy is preferred test
* Mesothelioma usually cannot be diagnosed from
pleural fluid and requires pleural biopsy

39
Q

Light’s Criteria

A

Light’s Criteria
Pleural fluid is an exudate if ≥ 1 of the following
criteria are met:
* Protein in fluid : serum > 0.5
* LDH in fluid : serum >0.6
* Pleural fluid LDH >2/3 the upper limit of normal
value for serum LDH.

40
Q

Pleural Fluid Differentials

A

Chylothorax – (TGs >1.24mmol, +CM)
– Malignancy #1 (most commonly lymphoma)
– Trauma/surgery, TB, LAM (young woman with cystic lung disease/PTX)

  • Pleural fluid eosinophilia - (>10%)
    – Etiology depends on history
  • Asbestos related (BAPE), drugs (ex. nitrofurantoin), malignancy (lung), infection (parasites), PE, eGPA
  • Low glucose - (glc<3, eff/serum<0.5)
    – Severity:
  • <1 mmol – RA, empyema
  • 1-3mmol – malignancy, TB, SLE

Lymphocytosis
– >80% TB vs lymphoma, TB often AFB negative and would suggest sputum AFB
* Pleural fluid ADA (adenosine deaminase) and IFN-gamma tests can suggest Tb (BTS 2023 – not widely
available)
* Tissue sampling for C&S gold standard for Tuberculous pleural effusion (BTS 2023)
– Carcinoma, yellow nail, sarcoidosis, RA

41
Q

Management of Parapneumonic Effusion

A

In case of suspicion of pleural infection, sample fluid if >1 cm on lateral decubitus
– US preferred in new guidelines but may see old question
* Inter costal drain needed if (does not need to be surgical chest tube):
– drainage of frank pus
– pH <7.2 [high risk of complicated parapneumonic effusion]
– pH 7.2-7.4 and LDH>900 (consider based on clinical scenario, glucose <4.0, pleural enhancement)
– If pH not available, glucose <3.3
– Rule out other potential causes of low pH. I.e. rheumatoid

Antibiotics should cover what is isolated
– Beta lactams preferred
– if no culture then treat for CAP plus anaerobes (empiric – and add anaerobic!)
* Usually prolonged antibiotic course (often at least 3 weeks, based on clinical and radiographic
response
– “2-6 weeks” per BTS, no RCTs to guide length
* Further treatments like intrapleural lytics and VATS require consultation with Resp or Thoracic Surgeon

42
Q

Primary Spontaneous Pneumothorax

A

Primary: Absence of underlying lung disease
* RF = smoking*, family history, Marfan syndrome, thoracic endometriosis
– Reoccur 25-50%, most in first year
* Conservative management for asymptomatic or minimally symptomatic patients (no significant
pain, breathlessness or physiological compromise)
– REGARDLESS OF SIZE OF Pneumothorax (New BTS 2023 … Beware old MCQs refer to 2cm cutoff)
* Conditional recommendation – conditional on reliable patient, close followup plan etc.

If symptomatic, look for high risk features: (tension, significant hypoxia, bilateral, >50 with
smoking history, hemopneumothorax).
– If present: Chest drain
* For all other patients: based on patient preference and local resources
– Conservative care, ambulatory device, needle aspiration OR chest drain.
* Close follow-up required for conservative care or ambulatory device (every 2-4 days). Follow-up
2-4 weeks for all

43
Q

Secondary spontaneous pneumothorax (SSP):

A
  • Secondary: presence of lung disease
  • COPD»> Others (CF, TB, PCP)
  • Even small SSP can lead to significant symptoms; often requires
    admission
  • Most likely will require chest drain given underlying lung
    abnormalities and risk of air leak. Unlikely to spontaneous
    resolve.
  • Consult Resp/Thoracic Surgery
44
Q

Sarcoid - definition

A

Multisystem granulomatous disease of
unknown etiology
– Pathology reveals noncaseating granulomas
in involved organs
– Usually involves the lungs (>90%) but up to
30% of patients present with
extrapulmonary sarcoid including:
* Heart, CNS, eyes* need urgent
treatment!
* Other: liver, spleen, musculoskeletal
system, kidney
* Most are asymptomatic
– Two thirds of patients will have remission at a
decade
– After one year of spontaneous remission
relapse is very uncommon

45
Q

Sarcoid Syndromes

A
  • Lofgren Syndrome
    – Bilateral hilar adenopathy
    – Erythema nodosum
    – Migratory polyarthralgias
    – Fever
    – Seen primarily in women
    – High likelihood of spontaneous remission

Heerfordt Syndrome
– Anterior uveitis
– Parotid enlargement
– Fever (uveoparotid fever)
– Facial palsy

46
Q

Sarcoid: Pulmonary Involvement Presentation

A

-90% have pulmonary involvement
– often asymptomatic hilar lymphadenopathy
* Stage reflects chance of spontaneous remission
* Symptoms can vary: dyspnea, cough, chest pain, wheeze
* PFTs can show anything: normal, restriction, obstruction, or both
(+/- reduced DLCO)
* Co-existent asthma is common
* Pulmonary hypertension is rare
but described

47
Q

Sarcoidosis: Extrapulmonary Involvement

A
  • Cutaneous: Common (about 1/3 of patients), lupus pernio, erythema
    nodosum, others
  • Liver and Spleen: ~10% of patients, elevated liver enzymes, cholestasis,
    rarely liver failure, can see liver and spleen lesions on imaging
  • Neurologic: Cranial nerve palsy, headache, ataxia, weakness, LP
    nonspecific lymphocytic inflammation, MRI imaging chest of choice
  • Ocular: Anterior uveitis most common
  • Cardiac: ~5% of patients clinically (more at autopsy), cardiomyopathy,
    arrhythmia, heart block, screen with ECG +/- echo, then cardiac MRI and
    PET scan if concern
  • Hypercalcemia: Common, rule out other causes of hypercalcemia, due to
    increased conversion of 25-OHD3 to 1,25-D3.
48
Q

Investigations for Sarcoidosis

A
  • CXR +/- CT, PFTs
  • Tissue biopsy: LN or transbronchial biopsy
  • CBC: anemia of chronic disease, lymphopenia, thrombocytopenia
  • Calcium, Alb, LFTs, Cr
  • ECG
    – If cardiac disease suspected – Cardiac MRI is preferred, or cardiac PET if unavailable
    – If PH suspected – do TTE
  • 1,25- OH Vitamin D
  • Ophtho referral to r/o sarcoid ocular
    Rule out: HIV serology, Rule out TB
  • Bronchoscopy/BAL: low CD8, elevated CD4/CD8 ratio
  • 24 hour urine (hypercalciuria)
  • Serum ACE level is not necessary
    – increased ACE is ~70% sensitive and 90% specific with active disease;
    – Reflects granulomatous load and can be false positive in other granulomatous disease
49
Q

Sarcoidosis Treatment

A

Most patients will not require treatment
– Most patients with stage 1 or 2 disease will have spontaneous remission, with low recurrence (4-5%)
– Steroids accelerate remission at the cost of higher risk of recurrence (60-70%) – indicated if end-organ failure from
granulomatous inflammation. Dose is 20-40 mg (higher if life threatening inflammation).

Indications for treatment

– Pulmonary: Bothersome symptoms (cough and dyspnea), deteriorating lung function as measured with PFTs, or
development of pulmonary hypertension. ICS can be used for mild symptoms and stable PFTs.
– Extrapulmonary: Eye disease, CNS disease, cardiomyopathy/active cardiac involvement *, severe skin disease,
hypercalcemia, symptomatic liver disease are usually treated (for skin disease refractory to steroids, consider
INFLIXIMAB)
* Duration of treatment
– Usually 1-3 months at initial dose, SLOW taper to ~10 mg/d (total treatment for 1 year)
– If relapse can consider other agents like MTX (less commonly HCQ, LEF, TNF alpha inhibitors)
* Erythema nodosum usually good response to NSAIDs alone
* Cutaneous sarcoid – if low burden can try topical steroids, intralesional steroids (Derm helpful here)
* Pulmonary rehab is 1st line treatment for fatigue.

50
Q

Pulmonary Hypertension- definition

A

Defined as: mean pulmonary artery pressure >20mmHg on right heart catheterization and PVR >2WU
(previously PVR > 3WU), is consistent with pre-capillary PH
– PVR = Pulmonary Vascular Resistance ((mPAP – PCW) / Q )
* PCW = Pulm Cap wedge P and Q = Cardiac output

51
Q

Pulmonary Hypertension- symptoms and work-up

A

– Hx: slowly progressive dyspnea on exertion and eventually right ventricular failure
* Suspect in dyspnea on exertion, isolated reduced DLCO
– Most important screening is echocardiogram – Assess how RV is doing!
* Initial work up directed at identifying PH etiology
– Classify into a WHO group (determines management)
* Everyone should get:
– CBC -lytes -LFTs -TSH -BNP screening connective tissue disease, viral hepatitis HIV
– Transthoracic echo -PFTs -6MWT
– CT pulmonary angiogram. ( + V/Q scan if unexplained PH to rule out CTEPH)
– Abdo US to screen for portal HTN
– sleep study if suspicious clinical features
– right heart catheterization

52
Q

Pulmonary Hypertension (groups/etiologies)- group 1

A

Group 1: (mPAP>20 with PVR > 2WU)
– Idiopathic (IPAH)
– Heritable
– Drug/toxin induced
– Associated with: CTD, HIV, portal HTN,
schistosomiasis
– (Group 1’: PVOD)
Pulmonary veno-occlusive disease is a rare cause of group 1 pulmonary hypertension. It is characterized by having significant venous and capillary involvement, as opposed to other causes of group 1 pulmonary hypertension, in which the arteries are primarily involved.

Most patients will present with signs of right-sided heart failure, such as leg edema, ascites, and volume overload. They often will complain of dyspnea on exertion and orthopnea. Physical findings in these patients may include a split S2, loud P2, crackles, and cyanosis.This reflects the worsening right ventricular dysfunction.

TREATMENT: Should be referred to a PH centre
– Vasoreactivity testing to determine if candidate for CCB

– PDE5 inhibitor or riociguat (soluble guanylate cyclase nhibitor)

– Endothelin receptor antagonist-
-ambrisentan (Volibris)
-bosentan (Tracleer and now “generic” i.e. not branded)
-macitentan (Opsumit)

– Prostanoid

– Influenza/pneumococcal/COVID etc vaccines
– Supervised Exercise
– Women – pregnancy counselling (avoid pregnancy)

53
Q

Pulmonary Hypertension (groups/etiologies)- group 1

A

Group 2:
– Pulmonary hypertension due to left heart disease
* Systolic dysfunction, diastolic dysfunction, valvular
disease
* Treat underlying cause
Group 3:
– Due to lung disease/hypoxemia (COPD, ILD, etc)
– Treat underlying cause
Group 4
– Chronic thromboembolic pulmonary hypertension
APLAS testing for all. If + à warfarin (ERS 2022)
Refer for pulmonary thromboendarterectomy,
anticoagulation
Group 5:
– PH with unclear mechanisms – Treat underlying disease
* Heme disorders (myeloproliforative disease,splenectomy)
* Systemic disorders (sarcoid, LCH, LAM)

54
Q

Key notes from pulmonary HTN guidelines

A

Notes from this guideline applicable to GIM: – Screen patients with scleroderma annually for PH
with echo and DLCO
– Echo to screen for PH in patients with portal
hypertension undergoing transplant w/u
– If dyspnea or exercise intolerance after at least 3
months of uninterrupted anticoagulation post acute
PE assess for CTEPH with echo and V/Q lung scan
– Patients with CTEPH
– test for APLAS

55
Q

Clues for PH on ECHO

A

RVSP (not a hard cutoff/not sensitive) but ≥40 mmHg
”RV enlargement” “RV overload” “IVS flattening”, or TR jet
velocity ≥ 2.8, TAPSE < 1.7 cm, FAC < 35% – GIM do not
need to know ECHO criteria, just when to suspect/refer.

56
Q

ERS Guideline pulmonary HTN

A

Echocardiography recommended first-line non-
invasive diagnostic investigation in suspicion of PH

VQ Scan recommended in unexplained PH to
exclude CTEPH

Routine biochem, CBC, immunology, HIV testing
and TSH recommended in all patients with PAH to
identify an associated condition

Abdo U/S recommended to screen for portal htn I C
PFT + DLCO recommended in the initial evaluation
of patients with PH

Patients with Scleroderma should be evaluated
annually for the risk of PH.

In patients with SSc and unexplained dyspnea
following non-invasive assessment, RHC is
recommended to exclude PAH

Consider HRCT in all patients with PH

Pulmonary angiography should be considered in
workup of CTEPH

Open/thorascopic lung biopsy not recommended
in PAH

57
Q

Hypoxemia Approach

A

A-a = [150- (PaCO2/0.8)]– PaO2

Approximate Normal A-a Gradient for reference: (Age (yrs)/4)+4

Normal A-a gradient (normal gas exchange)
– Hypoventilation
* CNS depression (drugs, stroke, tumour, bleed, meningitis), spinal cord injury, chest wall
abnormality, diaphragm dysfunction (ie phrenic nerve injury or myopathy), neuromuscular
disorder, obesity hypoventilation
* Check PaCO2 – if elevated think of hypoventilation
– Low inspired FiO2 (e.g. altitude)

Widened A-a gradient
– V/Q mismatch (improves with 100% FiO2)
* E.g. COPD, PE

– Shunt (does not improve completely with administration of 100% FiO2)
* CAUSE: intracardiac with R->L shunt (eg PFO, ASD, VSD), intrapulmonary (ie pulmonary AVM),
physiologic (ie severe pneumonia with perfused alveoli that are not ventilated)

– Diffusion Abnormality
* E.g. ILD

58
Q

Hypoxemia- When to prescribe Home 02

A

When to prescribe Home O2
PaO2 ≤ 55 (ie on ABG) or
(Resting SaO2 ≤ 88%) or
PaO2 = 55-59 with:
* Cor pulmonale or
* Pulmonary hypertension or
* Persistent erythrocytosis (Hct >55%)

59
Q

Respiratory Blood Gases

A

RESPIRATORY ACIDOSIS
Reflects a decrease in alveolar ventilation.
If marked limitation in pulmonary reserve (increased deadspace), or hypoventilation will lead to consequent acidosis.

RESPIRATORY ALKALOSIS

Reflects an increase in alveolar ventilatio (i.e., pain, fever, anxiety, liver disease, pregnancy)
In the presence of mechanical ventilation, decreased carbon dioxide production (i.e., sedation, skeletal muscle paralysis,hypothermia) can cause respiratory alkalosis.

60
Q

Hemoptysis

A

-See nice approach to hemoptysis chart

  • Massive (variable definitions; ~200-600 cc/24 hours)
    – Acute management à Airway, Breathing, Circulation
    – If able to localize bleeding side
  • position patient in decubitus position to protect unaffected lung
    – Hold anti-coagulation/ correct coagulopathy
    – CBC, coagulation profile, ABG
    – Cross-type, IV fluids, oxygen
  • Investigations
    – Need imaging if patient is stable enough (CXR/CT)
    – Flexible bronchoscopy can be used for localization prior to IR guided embolization
  • Management dependent on local center
    – Interventional Radiology – Arterial embolization #1 if available
    – Thoracic Surgery – Ability for rigid bronchoscopy/Resection
    – Patients die of asphyxiation NOT exsanguination
61
Q

Cough Approach

A
  • CXR and exclude ACE-inhibitors
  • In this order, test and treat for:
    – UACS
  • Confirmed by response to Tx with 1st generation antihistamine/ decongestant (bronpheniramine/SR
    pseudoephedrine)
  • Sinus imaging if does not improve

– Asthma
* Methacholine challenge and/or empiric ICS (may treat NAEB as well)

– GERD
* If “clinical profile” fits (not necessarily GI symptoms), treat empirically
– Lifestyle: coffee, chocolate, citrus, smoking ,etc.
– H2RA/PPI
– Prokinetic
* 24h pH monitoring on therapy if cough persists
* Antireflux surgery if refractory

– NAEB
* Sputum eosinophils, if available, or an empiric trial of corticosteroids

62
Q

Obstructive Sleep Apnea- defintion

A

Defined by presence of both:
– Symptoms (sleepiness, choking, awakenings etc) and
– Objective testing (> 5 apnea/hypopnea events during sleep monitoring)
* Mild 5-15 (events/h) / Moderate 15-30 / Severe >30

63
Q

Obstructive Sleep Apnea- Treatment

A

Treatment Indications
– Patients with symptoms of excessive sleepiness or impaired sleep-related QOL
– Comorbid HTN
– Asymptomatic patients with severe OSA

Treatments
– Weight loss (see endocrinology Bonus slides re Obesity)
– PAP (CPAP or APAP)
* All patients should be offered therapy, asymptomatic patients should be treated if
have comorbidities (ie. HTN), AHI >30, critical occupation
– Oral appliances – for mild-moderate disease
– Surgery (rare) – Tonsillectomy if appropriate, uvulopalatopharyngoplasty in select
patients

64
Q

Driving Guidelines- For Sleep apnea

A

Severity of OSA alone is not a reliable predictor of collision risk and
should not be used in isolation to assess fitness to drive
* Consider co-morbidities, meds, sleep schedule and history of collisions in
addition to severity
* Mostly up to respirologist discretion in non-commercial drivers.
* In commercial drivers with AHI > 20, patients generally need to be
“treated adequately” i.e. compliant with therapy
– Defined as >= 4hrs >70% of nights in past 30 days

65
Q

Spirometry (PFT) approach

A

obstructive lung disease - flattened curve (expiratory flow decreased)

Restrictive lung disease - flattened upper and lower curve = (exp and inspiratory flow decreased)

Neuromuscular weakness - circle

Spirometry:
* Is there Obstruction? (FEV1/FVC<LLN)
– If yes, is it reversible or fixed (FEV1 >12% + 200cc)?
– Is there reduction in FVC suggesting restriction or gas trapping

66
Q

Diaphragmatic Weakness

A
  • Often idiopathic, often unilateral (and may be entirely asymptomatic)
  • Causes include:
    – Trauma or surgery (C3-5 injury during trauma, phrenic nerve injury during cardiac surgery)
    – Mechanical ventilation
    – Myopathy/neuropathy
  • ALS, MG, critical illness myopathy/neuropathy

@IMR we often get asked: What is the most specific and most sensitive test
for diagnosis of diaphragm weakness/paralysis?

Most SENSITIVE = MIP.
Most SPECIFIC: There isn’t really a good specific test on PFTs for
diaphragmatic weakness. Proceed to ultrasound if you want specificity. If
forced to choose we “guess” FVC… because it’s associated with poor
prognosis in diaphragmatic dysfunction as per the ALS CTS guidelines.