Download B2B Respirology Review 2011 Dr Voduc

Back to Basics Review:
Respirology in Under Two Hours
Nha Voduc MD FRCPC
Original Presentation by Jen Block MD FRCPC
April 8, 2011
The Plan...
• Pulmonary Function Testing
• Asthma
• COPD
• Sleep Apnea
• Pleural Effusion
• Lung Cancer
Spirometry: Measurement of Airflow
1. Take as deep a breath as possible
2. Blast out the air into spirometer
3. Continue exhaling for several more seconds
UpToDate
Flow Volume Loop
TLC
RV
Interpretation
• Upper Airway Abnormalities
• Obstructive Lung Disease
• Restrictive Lung Disease
Upper Airway Abnormalities
• Variable extrathoracic obstruction impairs inspiratory flow more than expiratory flow -negative pressure during inspiratory “sucks in” (narrows) airway
• Variable intrathoracic obstruction impairs expiratory flow more than inspiratory flow -positive intrathoracic pressure compresses in airway
ERJ 2005; 26: 948-968
Obstructive Lung Disease
• FEV1/FVC is <70%
and
• FEV1 < 80%
(or < 2 standard deviations)
• “scooped out”
• lung volumes may show
Hyperinflation or “gas trapping”
(increased residual volume)
ERJ 2005; 26: 948-968
Restrictive Lung Disease
• TLC < 80% (or < 2 standard deviations)
• normal FEV1/FVC ratio
• Neuromuscular, Chest wall,
Interstitial Lung disease
ERJ 2005; 26: 948-968
Asthma
• Pathophysiology
• Diagnosis
• Chronic Management
• Acute Management
Asthma: Definition
• paroxysmal or persistent symptoms (dyspnea, chest tightness, wheeze,
cough)
• variable airflow limitation and airway hyper-responsiveness
• due to inflammation
Comprehensive Asthma Management
• Suspect asthma and confirm diagnosis
• Education
• Assess severity
• Avoid / control triggers and environmental modification
• Medications for chronic disease
• Assess control
• Management plan for exacerbation
• Regular follow-up
Asthma Diagnosis: Requirements PFTs
• If FEV1 is low, try to increase it using a short-acting bronchodilator
(reversibility)
• ≥12% and ≥180 ml improvement in FEV1 from baseline 15 minutes after the
use of an inhaled short-acting bronchodilator
Asthma Diagnosis
• If FEV1 is normal, try to see if airways are hyperresponsive by giving an
irritant (methacholine challenge)
Comprehensive Asthma Management
• Suspect asthma and confirm diagnosis
• Education
• Assess severity
• Avoid / control triggers and environmental modification
• Medications for chronic disease
• Assess control
• Management plan for exacerbation
• Regular follow-up
Asthma Management
Relievers – Short Acting Beta-Agonists
•
•
•
•
SABAs for acute relief
‘rescue’ medication used as needed
MDI salbutamol (Ventolin)
dry powder terbutaline (Bricanyl)
• Frequent use of SABA indicates poor control
• Regular use associated with tachyphylaxis
Asthma Management
Inhaled Corticosteroids (ICS)
• Anti-inflammatory ICS mainstay of therapy
– Prevent symptoms, improve PFTs, decrease hyper-responsiveness,
reduce morbidity
Inhaled Corticosteroids – How do they work?
• Like steroids produced endogenously by adrenal cortex
• Anti-inflammatory – inhibit production of cytokines, which:
– reduces eosinophil infiltration
– inhibits macrophage function
– reduces production of leukotrienes
Dosing Guide
Drug
Low Daily Dose (μg)
Medium Dose (μg)
High Daily Dose (μg)
Fluticasone
(Flovent)
≤250
251-500
>500
Budesonide
(Pulmicort)
≤400
401-800
>800
Beclomethasone
(Qvar)
≤250
251-500
>500
Ciclesonide
(Alvesco)
≤200
201-400
>400
ICS Adverse Effects
• thrush
• dysphonia
•
•
•
•
•
osteoporosis
decreased growth velocity (?)
glaucoma
cataracts
adrenal insufficiency
Asthma Management
Long Acting β2-Agonists (LABAs)
• add if not controlled by moderate dose ICS
• better than doubling ICS
• “not recommended as maintenance monotherapy”
– Increased mortality!
• doesn’t replace SABAs
• salmeterol (Serevent), formoterol (Oxeze)
Combination LABA / ICS Products
– Salmeterol/fluticasone (Advair) MDI and diskus
– Budesonide/formoterol (Symbicort) turbuhaler
Leukotriene Receptor Antagonists (LTRAs)
• Second or third choice medication or in patients who can’t take ICS
• Montelukast (Singulair)
• Oral medication
• Use in patients with:
– symptoms despite LABA/ICS
– ASA sensitivity, nasal polyps
– exercise-induced asthma
IgE Antagonists: Omalizumab (Xolair)
•
Monoclonal antibodies block action of IgE on mast cell
•
Effective if IgE levels are only slightly elevated (500-1200)
•
Monthly injection
•
Extremely expensive
•
Use if frequent need for oral steroids despite optimum
conventional Rx and patient has drug plan or $$$
Comprehensive Asthma Management
• Suspect asthma and confirm diagnosis
• Education
• Assess severity
• Avoid / control triggers and environmental modification
• Medications for chronic disease
• Assess control
• Management plan for exacerbation
• Regular follow-up
Assess Control
• Both physicians and patients over-estimate their degree of control
(many patients are much worse than they think they are)
Comprehensive Asthma Management
• Suspect asthma and confirm diagnosis
• Education
• Assess severity
• Avoid / control triggers and environmental modification
• Medications for chronic disease
• Assess control
• Management plan for exacerbation
• Regular follow-up
Asthma Exacerbation
• ABC’s
– include RR, O2 sats, assess work of breathing, wheezing
• history:
– Diagnosis
– Environmental triggers
– Previous exacerbations/admissions/intubations
– Treatment history
• Compliance
• Inhaler technique
– Other medical illnesses or medications
Asthma Exacerbation
• short-acting beta-agonists
ie. salbutamol (Ventolin)
• short-acting anti-cholinergics ie. ipratropium (Atrovent)
• systemic anti-inflammatory therapy
– oral = prednisone
– intravenous = solumedrol
• very severe: MgSO4, intubation, anesthetic
COPD
• Definition
• Constrast from asthma
• Pathophysiology
• Diagnosis
• Chronic Management
• Acute Management
COPD Definition
• respiratory disorder largely caused by smoking characterized by:
- progressive, partially reversible airway obstruction
- hyperinflation
- systemic manifestations
- increasing frequency and severity of exacerbations
COPD Risk Factors
• Host Factors:
- genetics (alpha-1-antitrypsin deficiency)
- bronchial hyper-responsiveness
• Environmental Factors:
- smoking
- childhood viral infections
- occupational & environmental exposures
Pathophysiology - Airflow Obstruction
• alveoli and support structures are destroyed
– decreased elastic recoil
– lack of tethering gives airway collapse
• airway compression by adjacent overdistended lung units
• mucosal inflammation and secretions
Pathophysiology - Hyperinflation
• expiratory flow limitation in COPD
results in air trapping
• end-expiratory lung volumes are
increased
• further hyperinflation with exercise
(increased respiratory rate results
in decreased expiratory time)
• decreased inspiratory capacity a
major cause of dyspnea
– Increased load on inspiratory
muscles
COPD Diagnosis
• do not screen asymptomatic individuals
• assess symptomatic patients with spirometry
• post-bronchodilator FEV1/FVC ratio less than 0.7
COPD Stage
Post-bronchodilator FEV1
(% predicted)
mild
≥ 80
moderate
50 - 79
severe
30 - 49
very severe
< 30
COPD Management
Education - Effects of Smoking on FEV1
Mortality Benefit
BMJ 2008; 336: 598-600.
Education
“Tobacco is the only legal consumer product that kills one
third to one half of those who use it as intended by its
manufacturers, with its victims dying on average 15 years
prematurely”
- World Health Organization
What Can You Do?
• 2007: 19% of adult Canadians are active smokers
• smoking cessation advice
– even brief advice increases chances of patients quitting
• Personalized, direct but non-judgmental message
– www.gosmokefree.ca
– www.smokershelpline.ca
• nicotine replacement therapy
– many different types
– any form of NRT increases chances of quitting vs. control
• buproprion, varenicline
Other Prevention
• vaccination:
– flu vaccine yearly
– pneumococcal vaccine q5years
COPD Management
Short-Acting Bronchodilators
• Even patients with “fixed” airflow obstruction can have good clinical
response to bronchodilators even if FEV1 changes very little
• Reduces hyperinflation, reduces dyspnea and increases exercise
capacity
Short-Acting Bronchodilators
• anti-cholingergics: ipatropium (Atrovent)
– dry mouth
– glaucoma if sprayed into eye
– urinary retention
• β2-agonists: salbutamol (Ventolin)
– tachycardia, palpitations
– sleeplessness, tremor
• improves PFTS, dyspnea and exercise performance
COPD Management
Long-acting anti-cholinergic
• tiotropium (Spiriva)
• once a day
• blocks M3 muscarinic receptors in bronchial
smooth muscle
• improves:
– PFTs, dyspnea, exercise capacity, quality of life
– decreases exacerbations
– maybe more improvement than LABA
Long-acting β2-agonist (LABA)
• salmeterol (Serevent) and formoterol (Oxeze)
• twice daily
• more sustained improvement in PFTs, dyspnea and QOL than shortacting bronchodilators
COPD Management
Dyspnea – Downward Spiral of Deconditioning
Dyspnea during
moderate exertion
Dyspnea during
mild exertion
Abstention
from exercise
Further
abstention
Dyspnea
during ADL
*
* = stay at home.
Depression, oxygen
therapy etc.
Respiratory
impairment
Further
deconditioning
Physical
deconditioning
Pulmonary Rehabilitation
– Exercise + psychosocial support
– Aerobic exercise + strength training
– improves dyspnea, endurance, QOL
– trend to decreasing mortality
– need a maintenance program
www.lungchicago.org
www.altru.org
COPD Management
Combination LABA / ICS Products
– Salmeterol/fluticasone (Advair) MDI and diskus
– Budesonide/formoterol (Symbicort) turbuhaler
– add to therapy if patient has persistent dyspnea or recurrent
exacerbations
– improve PFTs, QOL, decrease exacerbations
– Benefits much more modest than in asthma
COPD Management
Indications for long term oxygen therapy
• pO2 on room air of
≤ 55 mmHg
< 60 mm Hg if evidence of
– Polycythemia
– Cor pulmonale
– Right heart failure
• Mortality benefit
COPD Management
Surgery
• Lung Volume Reduction Surgery
- benefits patients with upper lobe (heterogenous) emphysema and
poor exercise capacity
• Lung Transplantation
-
single or double lung
non-smoker (must have quit smoking)
generally age< 65 without significant cardiac, renal, hepatic disease
post-transplant survival is 5-6 years on average
death from infection (early) and chronic rejection (later)
COPD Management
End of Life Issues
• Empathetic, realistic conversations about illness
• Opportunity to express wishes re: intubation
• Dyspnea
- morphine po, sc, iv
- benzodiazepines
• Cough
- opioids (codeine, morphine)
• Secretions
- scopolamine
What Decreases Mortality?
•
•
•
•
Non-Pharmacologic
Smoking cessation
Flu shot
Pneumonia vaccine
Pulmonary Rehab
Pharmacologic
Yes
No
No
?
• Oxygen
Yes
• Systemic Steroids
No
• Antibiotics
No
• SABA (Ventolin)
No
• Anti-cholinergics
No
• Theophylline
No
• Inhaled Steroids
No
• LABAs
No
• Combo ICS/LABA
No
COPD
• Contrast from asthma
• Definition
• Pathophysiology
• Diagnosis
• Chronic Management
• Acute Management
Acute exacerbations of COPD
• Over 50% are associated with a bacterial infection
• Decision to use antibiotics based on Anthonisen (Winnipeg)
criteria
• Antibiotics are helpful if there are at least two of:
– Increased dyspnea
– Increased volume of sputum
– Increased purulence of sputum
Acute exacerbations of COPD
• Treatment:
– ABCs
– O2 sat monitoring and oxygen prn
– history and p/e to rule out other causes of dyspnea
– CXR, ABG, sputum C&S
– Bronchodilators
– systemic steroids: prednisone 50 mg/d x 10-14 days (?)
– antibiotics if purulent sputum
– NIPPV
Antibiotics for Community Acquired Pneumonia
Obstructive Sleep Apnea Syndrome
• Elevated Apnea-Hypopnea Index on Sleep study (Polysomnography)
AND
• Nighttime Symptoms: Snoring, witnessed apneas
OR
• Daytime Symptoms: Morning headache, daytime sleepiness
Obstructive Sleep Apnea Syndrome
• Apnea Hypopnea Index (AHI):
–
–
–
–
normal
<5/hour
mild
5-15/hour
moderate 16-30/hour
severe
>30/hour
• Treatment:
–
–
–
–
weight loss, avoid sedatives
positional therapy (off supine)
Non-invasive positive pressure therapy: CPAP / BiPAP
oral appliance, UPPP, tracheostomy less common / less effective
Pleural Effusion
Pleural Fluid Accumulation
• In normal pleural space, the rate of fluid formation is balanced
by the rate of removal
• Rate of fluid formation is determined by the Starling equation
– hydrostatic forces push water out of vessel
– osmotic forces pull water back into vessel
• Pleural effusion is due to abnormalities in one of these
processes
Pleural Effusion Evaluation
• Cell count and differential
• Gram stain
• Culture
• AFB
• Cytology
• LDH
• Total protein
• Glucose
• pH
Pleural Effusion Evaluation
Light’s Criteria
• pleural fluid protein/serum protein > 0.5
• pleural fluid LDH / serum LDH > 0.6
• pleural fluid LDH > 2/3 upper limit normal LDH
Any of these three criteria means fluid is EXUDATE
Pleural Effusion Etiology
Many!
Transudate = fluid overload or reduced oncotic pressure (low albumin)
heart, liver, kidney
Exudate = infectious
inflammatory
malignant
iatrogenic
Pleural Effusion Etiology
• If exudate with no determined cause, you want to rule-out malignancy
CT chest with contrast
pleuroscopy or VATS
bronchoscopy
follow / repeat thoracentesis
Malignant Pleural Effusions
 Treatment is palliative (reduce symptoms associated with
effusion)
Cure generally not possible
In most cases, effusion will persist despite chemotherapy
 Most
places, patients admitted for symptomatic thoracentesis +/tube drainage and pleurodesis (talc)
 In
Ottawa, patients mostly receiving PleurX (indwelling) catheters
to allow home drainage
Solitary Pulmonary Nodule
 Many
causes - both benign and malignant
Infectious granulomas
fungal
tuberculous
Benign neoplasm
hamartoma
lipoma
Vascular
AVM
Developmental
Bronchogenic Cyst
Inflammatory
Wegener’s
Bronchogenic Cancer
SCLC
NSCLC - adenocarcinoma
squamous
large cell
carcinoid
Metastatic Cancer
breast
colon
others...
Solitary Pulmonary Nodule
 Many
causes - both benign and malignant
 Clinical (age, smoking
history) and radiographic features help
Benign
Malignant
Size
smaller (<1 cm)
larger (>3 cm)
Margins
round, smooth
irregular
spiculated
Over time
stable
growth
Calcification
popcorn, central
concentric, diffuse
None or asymmetric
Solitary Pulmonary Nodule
 Management depends on
risk of maligancy
 Options:
Ignore
Follow
(repeat imaging within 3-6 months)
Biopsy
Resect (almost
never done without first attempting biopsy)
Small Cell Lung Cancer
• Approximately 20% of lung cancers
• more rapid doubling time, earlier metastases
• responsive to chemotherapy and radiation
but quickly relapses
•
•
•
•
smokers
central airways
present with metastases
paraneoplastic syndromes
PEIR Digital Library http://peir2.path.uab.edu
Small Cell Lung Cancer
• Limited (30-40%): involves only one hemithorax (maximum
allowable for radiation portal)
- concurrent chemo + radiation
- median survival 15-20 months
- (very small chance of cure)
• Extensive (60-70%): extends beyond hemithorax
- Chemotherapy only
- median 8-13 months
- (cure not possible)
PEIR Digital Library http://peir2.path.uab.edu
Non Small Cell Lung Cancer
• 80% of all lung cancers
• 10-15% survival at 5 years
• staging by TNM system
T = tumour
N = node
M = metastases
Up To Date
www.utdol.com
Non Small Cell Lung Cancer
• Subtypes:
- Adenocarcinoma (now most common)
- Squamous cell carcinoma
- Large cell carcinoma
Bronchoalveolar Carinoma (BAC)
PEIR Digital Library http://peir2.path.uab.edu
Non Small Cell Lung Cancer
• Treatment and prognosis depend on stage
• Early Stage (1 or 2)
– Surgical resection if tolerated
– Adjuvant chemotherapy to reduce risk of recurrence
• Later Stage (3B or 4)
– Chemotherapy if performance status is reasonable
– Palliative Radiotherapy for symptoms
• Majority of NSCLC will not be resectable and/or operable
u
The Plan...
• Spirometry
• Asthma
• COPD
• Sleep Apnea
• Pleural Effusion
• Lung Cancer
Good Luck
• Questions?