Respiratory Mbchb4

ASTHMA

1. Definition
a. Chronic inflammatory condition of the lung airways
b. Three characteristics
i. Airflow limitation – often reversible, either spontaneously or with tx
ii. Airway hyper-responsiveness to a range of stimuli
iii. Airway Inflammation
2. Epidemiology
a. ↑ prevalence
b. 10-15% affected in 2nd decade of life
c. Common in NZ
3. Etiology – 2 major factors involved in devt of asthma
a. Atopy
i. Term used for individuals who readily develop IgE antibodies against common etal antigens (dust mite, grass pollen)
ii. Genetic and etal factors affect IgE levels
iii. Etal factors incl c/hood exposure to respiratory irritants such as tabacco smoke, intestinal bacteria and c/hood infections
iv. Growing evidence that growing up in a relatively clean evt may predispose towards IgE response to allergens
b. ↑ responsiveness of lung airways
i. as measured by a ↓ in FEV1
ii. to stimuli such as inhaled histamine and methacholine (bronchial provocation tests)
4. Classification
a. Traditionally divided into extrinsic (atopic) and intrinsic (non-atopic) asthma
b. On the basis that extrinsic asthma allergens can be identified by pos skin-prick reactions to common inhaled antigens
c. Now recognised that almost all asthmatic pts show some degree of atopy → classification less used now
5. Pathogenesis
a. Primary abnormality in asthma → airway narrowing
i. SM contraction
ii. Thickening of airway wall by cellular infiltration and inflammation (hypertrophy, edema)
iii. Secretions within airway lumen (mucus hypersecretion)
b. Complex and not fully understood
c. Involves a number of cells, mediators, nerves and vascular leakage which can be activated by several mechanisms
d. Inflammation
i. Cellular component of inflammatory response includes
1. Mmphages → initial uptake na dpresentation fo allergens to lymphocytes
2. T lymphocytes → release several types of CK → migration and activation of mast cells and Eosinophils
a. IL4 → antibody switching to production of IgE from B lymphocytes
3. Eosinophils → IgE molecules attach to mast cells → release of powerful mediators that act on SM and small blood vessels (mediators incl histamine) → immediate asthmatic reaction
4. Mast cells → activation of Eosinophils by IgE binding → release of mediators such as eosinophilic cationic protein (toxic to a/w cells)
e. Remodelling
i. A/w SM → hypertrophy (wall thickening)
ii. Epitheilium damage → metaplasia with ↑ numbers of goblet cells → ↑ mucus secretion
6. Precipitating Factors
a. Major allergen – fecal particles of house-dust mite
b. Non-specific factors which may cause wheezing
i. Viral infections
ii. Cold air
iii. Exercise
iv. Irritant dusts/vapours/fumes eg cigarette smoke, perfume, exhaust fumes
v. Emotion
vi. Drugs – eg NSAIDs, aspirin, b-blockers
c. Occupational – esp veterinary, bakery, laundry
7. Clinical Features
a. Sxs – non-specific to asthma and intermittent
i. Wheezing (does not necessarily indicate asthma)
ii. Coughing
iii. Chest tightness
iv. Shortness of breath
v. Sxs are non-specific to asthma, intermittent, worse at night, provoked by triggers
vi. Some pts have only 1-2 attacks/year while others suffer from chr asthma
vii. Assessing asthma control → a. salbutamol inhaler use, b. night waking, c. exercise tolerance
viii. Reasons for poor asthma control →
1. non-compliance – incorrect inhaler use or not taking inhaled steroid on regular basis
2. etal/occupational/domestic factors
b. Signs (during an attack)
i. ↓ chest expansion
ii. Prolonged expiratory time
iii. Bilateral expiratory polyphonic wheezes
8. Differential Dx
a. COPD
i. Asthma reversible, COPD not reversible
ii. Green sputum can still occur in asthma
iii. COPD generally 50’s or older and smoking hx
iv. Test sputum for Eosinophils in asthma
v. Measure exhaled NO in asthma
vi. Steroid trial ineffective in COPD
b. Bronchiectasis
c. Bronchiolitis (small a/w dis)
d. Large a/w obstruction – eg endobronchial tumor, extrinsic compression, foreign body
e. Hyperventilation syndrome
f. Functional laryngeal spasm
g. LVF
h. DILD
9. Ixs
a. Dx often made on hx and response to bronchodilators → No single diagnostic test for all pts
b. Demonstration of variable airflow limitation → Spirometry
i. FEV1 - 15% ∆ and >200 ml
ii. ↑ PEFR after inhalation of bronchodilator eg salbutamol
iii. ↓ after 6 mins of exercise
c. PEFR
i. Not a substitute for spirometry
ii. Effort dependent
iii. Considerable inter-instrument variability
iv. Wide normal range
v. Measurement of PEFR by pt on waking, during day, before bed → most asthmatic individuals show diurnal variation (lowest values early in morning)
vi. PEFR - 20% ∆ from baseline and >60 L/min
d. Histamine or methoacholine challenge in difficult cases (hypertonic saline)
i. Bronchial hyper-reactivity when pt inhales gradually increases doses of histamine
ii. ↓ in FEV1 demonstrated
iii. Test should not be performed on individuals with poor lung function (FEV1 < 1.5L) or a hx of brittle asthma
e. Measure exhaled NO (iNOS in asthma)
i. Expired nitric oxide
ii. Eosinophilic a/w obstruction
iii. Dx and response to steroids
f. Skin prick tests
i. To identify allergens to which the pt is sensitive
ii. Weal develops 15 mins after allergen injection into epidermis of forearm
g. CXR
i. Performed at dx
ii. Only repeated in severe asthma attack
h. Steroid trial
i. Prednisone 30mg daily for 2 weeks
ii. Should be given to all pts w severe airflow limitation
iii. Improvement of FEV1 >15% confirms some reversibility and indicates that inhaled steroids may prove beneficial
10. Management
a. General
i. Family education
ii. Flu vaccine
b. Avoidance of precipitating factors
i. Ø smoking
ii. ?Pets
iii. Frequent house cleaning and effective bedding covers
iv. Occupational – early dx and avoidance may cure asthma whereas continued exposure may lead to severe asthma which continues when exposure ceases
v. B-blockers are contraindicated
c. Drug tx
i. B2 agonists → relax bronchial SM → bronchial dilation
1. Salbutamol (SABA) (ventolin – blue inhaler) → onset 5 mins, duration action 4-6 hrs
a. Side effects → tremor, tachycardia (↓ as tolerance develops; airways less effected by down-regulation due to higher density of receptors)
2. Terbutaline
ii. Antimuscarinic bronchodilators
1. Ipratropium bromide → may be additive to adrenoceptor stimulation
iii. B2 Agonists – LABAs (add on only)
1. Salmeterol (serevent)
2. Eformeterol (oxis)
3. BD dosing – duration action 12 hrs
iv. Corticosteroids – tx of underlying inflammation
1. Powerful anti-inflammatory agents
2. Regular use required
3. Days/weeks required for full effect
4. Inhaled steroids → maintenance tx in all but v mild asthmatic case, if salbutamol use >1 /day
a. Beclometasone (Beconase – brown) – 200 ug BD
b. Budesonide – 200 ug Bd
c. Fluticasone (Flixitide – orange) – 50/125 m=ug BD
d. Side effects – oral candidiasis, hoarseness, cataract formation (rare)
e. ↑ dose as needed to a maximum of 2000 ug daily
v. Combined medications
1. Symbicort (red) → budesonide + eformeterol
2. Seretide (purple) → fluticasone + salmeterol
vi. Oral Steroids - occasionally necessary in those pts not controlled on inhaled steroids
vii. Theophylline
1. Inhibition of PD (phosphodiesterase) breakdown of cAMP → ↑ cAMP → bronchodilation
2. Problems
a. Narrow therapeutic range
b. Side effects – N/V, headache, insomnia, tachycardia, palpitations, seizures, arrhythmias
3. Start w low dose, wait 3 days then check levels
4. If no side effects and below therapeutic range → ↑ the dose (double the dose = double the conc)
viii. Leukotriene R antagonists (LTRA) eg montelukast (not available in nz)
1. leukotrienes are inflammatory mediators released by mast cells which cause bronchoconstriction and ↑ mucus production
2. useful in pts still w sxs despite high dose inhaled or oral corticosteroids
ix. Methotrexate in low doses → steroid sparing agent in severely asthmatic individuals
x. IV aminophylline – occasionally used in acute severe asthma
d. Stepwise management of chr asthma in adults
i. Pt measures PEFR at home to guide tx
ii. SABA taken at any step as needed for sx relief
iii. Rescue of oral steroids may be needed at any time and at any step
iv. Check inhaler technique and competence before ↑ in tx
v. ↓ tx after 1-3 months of stability
vi. Steps
1. Step 1 – Mild intermittent Asthma
a. Inhaled SABA PRN
2. Step 2 – Regular preventative therapy
a. Symptomatic >2x /week or night waking → add inhaled steroid
3. Step 3 – Add on therapy
a. Add inhaled LABA
4. Step 4 – Persistent poor control
a. ↑ inhaled steroid to 2000 ug/day and/or
b. addition of 4th drug → LTRA, SR theophylline
5. Step 5 – Oral steroids
a. Continuous or frequent use at lowest possible dose

Acute Severe Asthma

1. Diagnosed when pt has severe progressive asthmatic sxs over a number of hours/days
2. Medical emergency and treated immediately at home with subsequent transfer to hospital
3. Can lead to death
4. Clinical features
a. Inability to complete a sentence in one breath
b. RR >25 /min
c. Tachycardia >110 bpm
d. PEFR 33-50% of predicted value or pts best
5. Life threatening features
a. Silent chest
b. Cyanosis
c. Feeble respiratory effort
d. Exhaustion
e. Confusion or coma
f. Bradycardia
g. Hypotension
h. PEFR <30% of predicted or best (~150 L/min in adults)
i. Blood gas markers – PaO2 <8 kPa, SpO2 <92% despite O2 tx
6. Management of moderate asthma presentation
a. Moderate asthma (PEFR 51-75%) → nebulised b-agonist; may be discharged after 1 hr of stability with a tapering dose of prednisone (starting at 40 mg daily); continue oral prednisone until acute attack completely resolved

COPD

1. Definition
a. Aka CORD, COAD
b. 2 part definition
i. Group of diseases characterised by airflow limitation in the airway that is not fully reversible
ii. Airflow limitation is progressive and associated with an inflammatory response of the lungs to noxious gases
c. Includes emphysema and chronic bronchitis – in reality, most pts will have feats of both
d. COPD now the preferred term for pts w airflow obstruction who were previously diagnosed as having either chr bronchitis or emphysema
e. Most often due to smoking, but can be caused by other airborne irritants such as coal dust, asbestos or solvents
2. Epidemiology
a. 5% of adult population
b. 4th most common COD
c. 60% of pts require readmission to hospital <1yr
3. Etiology and Pathophysiology
a. Smoking → activation of mphages + airway epith cells → release of neutrophil chemotactic factors
b. Neutrohils + mphages release proteases → breakdown of CT in lung parenchyma → emphysema + stimulation of mucus hypersecretion
c. Proteases normally countered by protease inhibitors (incl a1-antitrypsin) – In COPD → tipped in favour of proteolysis
d. A1-antitrypsin deficiency is a rare cause of early onset emphysema
4. Clinical Features
a. Sxs
i. Cough
ii. Sputum production
iii. Wheeze
iv. Dyspnea
v. Frequent infective exacerbations → purulent sputum
b. Signs
i. Breathless at rest
ii. Prolonged expiration using accessory respiratory muscles (SCM, scalenes)
iii. Poor chest expansion
iv. Hyper-inflated lungs
v. Wheeze or quiet breath sounds
vi. Pink puffers → breathlessness = predominant sx (Ø cyanosis)
vii. Blue bloaters → hypoventilate, cyanosis + edematous features
1. Feats of CO2 retention → warm peripheries, bounding pulse, asterixis, confusion
5. Investigations
a. No single diagnostic test for COPD
b. Dx made on hx, exmn + confirmation of airflow limitation with lung function testing
c. Lung function tests
i. ↓ FEV1 → <80% of predicted
ii. ↓ FEV1/FVC ratio → <0.7
iii. Some pts have partially reversible airflow limitation with ↑ in FEV1 (<15%) following B2 agonist inhalation
iv. If doubt, further testing may show lung vols normal or ↑
d. CXR
i. Hyperinflated lungs – low flat diaphragm, long narrow heart shadow, ↓ peripheral lung markings and bullae
ii. Can be normal
e. HB and PCV
i. ↑ HB and PCV – due to persistent hypoxaemia with 2ndry polycythemia
f. ABG
g. ECG/Echo – if features of cor pulmonale
6. Differential Dxs
a. Asthma
i. Consider COPD rather than asthma when age of onset >35 yrs, smoking hx, chr dyspnea, sputum production, no marked day-to-day FEV1 variation
b. Lung ca
c. Bronchiectasis
d. HD
e. ILD

Chronic Bronchitis (blue bloater)

1. Definition
a. Cough + excessive mucus production (>5ml)
b. >3 months in at least 2 consecutive years
c. Not due to any other disease/condition
d. “Clinical Diagnosis”
2. Pathology
a. Enlargement of mucus glands → mucus hypersecretion → obstruction
b. Irritation → Inflammation + Edema → scarring + remodelling → wall thickening → airway narrowing
c. Superadded infection
d. Progression = mucobronchitis → mucopurulent bronchitis → chronic wheezy bronchitis (obstruction)
3. Presentation
a. Sxs
i. Dyspnea
ii. Productive cough
iii. Frequent respiratory infections that worsen sxs
iv. Fatigue
b. Signs
i. Cyanosis (↓ Hb sat)
ii. Edema/Congestion (bloating) – due to loss of hypercapnic drive → cor pulmonale
iii. Asterixis (CO2 retention)
iv. Plethoric face (polycythema 2ndry to chr hypoxia)
v. Wheeze
vi. Crackles
4. Investigations
f. Pulse oximetry
g. FBC
h. ABGs
i. ↓ PaO2, ↑ PaCO2
i. Spirometry
i. ↓ FEV1, ↑ FVC → ↓↓ FEV1/FVC Ratio
j. CXR
5. Complications
a. Early cor pulmonale
b. Acute bronchitis
c. Pneumonia
d. Emphysema
e. Respiratory failure
f. Cardiac arrhythmia

Emphysema (pink puffer)

1. Definition
a. Enlarged air spaces distal to terminal bronchioles with destruction of alveolar wall
b. “Histological Diagnosis”
2. Pathology
a. ↑ elastase activity → destruction of alveolar walls → enlargement of air spaces (↓ recoil)
b. ↓ surface area → ↓ O2 transfer
c. ↓ elasticity → dyspnea
d. Small airways collapse during expiration → obstruction to airflow
e. Excess work of breathing → more responsive to hypercapnic drive → hyperventilation allows maintenance of almost normal ABGs
3. Presentation
a. Sxs
b. Signs
i. Tachypnea
ii. ↓ I/E Ratio
iii. Pursed lip breathing – chest cant expand, pt uses chest wall to collapse the airway → ↑ pres forces air out
iv. Thin - ↑ rate of work
v. Anxious
vi. SCM and accessory respiratory muscle hypertrophy
vii. Tracheal tug
viii. Hyperinflated chest (AP diameter)
ix. Intercostal and subcostal indrawing
x. ↓ chest expansion
xi. Loss of cardiac and liver dullness
xii. Hyper-resonance
xiii. ↓ breath sounds
4. Ixs
a. ABGs → almost normal; may have ↓ PaO2, ↓ PaCO2
b. Spirometry → ↑ TLC, ↓ FEV1
5. Management
6. Complications
a. Late cor pulmonale

Cor Pulmonale

1. Defintion
a. R HF due to chr pulmonary HTN
2. Etiology
a. Chr lung dis (COPD → extra work reqd by heart to pump blood through the lungs)
b. Pulm vascular d/os
c. Neuromuscular d/os
d. Skeletal d/os
3. Presentation
a. Sxs
b. Signs
i. ↑ JVP
ii. Pulsatile liver
iii. Edema
iv. Murmur – pan-systolic at parasternal border, louder on inspiration
4. Investigations
a. FBC – ↑ Hb, ↑ haematocrit (due to 2ndry polycythemia)
b. ABG – hypoxia w or w/o hypercapnia
c. CXR – enlarged RA/RV, prominent pulmonary arteries
d. ECG – R axis deviation, RVH

Respiratory Failure (aka respiratory acidosis)

1. Definition
a. Type 1 - ↓ O2 <6 (10-13 normal)
b. Type 2 - ↑↑ CO2
2. Both chr bronchitis and emphysema → respiratory failure
3. Presentation
a. Signs
i. ↑ CO2
ii. Anxiety
iii. Confusion
iv. Delirious
v. Agitation
vi. Lethargy
vii. Coma
viii. Asterixis
ix. Muscle twitching
x. Babinski reflex
4. Hypoxia Sxs
a. Dyspnea
b. Restlessness, Agitation
c. Confusion
d. Central cyanosis
5. Hypercapnia Sxs
a. Headache
b. Peripheral vasodilation
c. Tachycardia
d. Asterixis
e. Papilloedema
f. Confusion
g. Drowsiness
h. Coma

Why hospital now?

1. Infection!!!
2. Cor pulmonale
3. Respiratory failure
4. Arrhythmia (AF) – 1/3 pts eventually
5. Pneumothorax
6. Lung ca (smoking)
7. PE
8. Natural hx of disease – progression
9. Poor compliance with meds

Management of COPD

1. Treat infection → Antibiotics
2. Non-pharmacological
a. Ø smoking → nicotine replacement, behal intervention
b. Exercise
c. Obesity tx
d. Influenza/pneumococcal vaccination
e. Pulmonary rehab
3. Pharmacological
a. Mild
i. Muscarinic (M3) antagonists → Ipratropium (or Tiotropium) PRN → a/w SM relaxation
ii. OR B2 inhaled agonist → Salbutamol (SA) Salmeterol (LA) PRN
b. Moderate
i. Regular Ipratropium or B2 agonist
ii. +/- Inhaled steroid → fluticasone, budesonide, beclomethasone
1. Seretide = salmeterol + fluticasone
2. Symbicort = budesonide + eformoterol
iii. Oral theophylline
c. Severe
i. Combination therapy
ii. Regular short acting B2 agonist
iii. Anti-cholinergic
iv. Steroids
v. Home nebulisers
4. Treat associated problems
a. Cor pulmonale → diuretics
b. Arrhythmias → rate control
5. COPDX Plan
a. Confirm dx and assess disease severity
b. Optimise function
i. Inhaled bronchodilators (sx relief)
1. SABA → Salbutamol or Ipratropium
2. Inhaler technique
ii. LA bronchodilators (moderate to severe COPD)
1. LABA → Salmeterol or Tiotropium
iii. Inhaled glucocorticoids (eg fluticasone) for severe COPD w freq exacerbations
iv. Systemic glucocorticoid LT use not recommended)
v. Pulmonary rehab
c. Prevent deterioration
i. Smoking cessation
ii. Influenza/pneumococcus vaccination
iii. LT O2 therapy – 15 h/day in hypoxaemic pts (PaO2 <7.3 kPa) – high flow O2 may worsen CO2 retention in pts w lost hypercapnic drive
d. Develop support network and self mgt plan
i. Pulmonary rehab → breathe deeply + slowly to prevent collapse
e. Manage exacerbations
i. Antibiotics → cefaclor or co-amoxiclav (if hx of purulent sputum or CXR changes
ii. Systemic glucocorticoids in acute exarcerbations only – oral prednisone 30mg OD 2wks
iii. Non-invasive pos pres vent is effective for acute hypercapnic ventilatory failure
iv. Controlled O2 delivery – 28% or 0.5-2 L/min indicated for hypoxaemia

DIFFUSE PARENCHYMAL LUNG DISEASE

1. Defintion
a. Known commonly as ILD (interstitial lung disease)
b. Inflammation of the pulmonary interstitium w or w/o progression to fibrosis
c. 200+ diseases – some systemic, some confined to the lungs
2. Aetiologies of ILD
a. Idiopathic eg pulmonary fibrosis
b. Environmental – eg asbestosis, extrinsic allergic alveolitis
c. Drug – eg amiodarone, methotrexate
d. Systemic dis – eg interstitial pn as part of a CT d/o such as rheumatoid, SLE, scleroderma
e. Genetic – eg interstitial accumulationof lipoid material in neiman pick disease
f. Other – eg sarcoidosis
3. The ILD patient
a. Usually older and may have other co-morbidities (exception is sarcoidosis)
b. Insidious onset of dsypnea and dry cough
c. Ø wheeze
d. May have had failed tx for inf and HF (main differential dxs)
e. May be asx and present with abnormal CXR only
4. Hx
a. Dyspnea duration?
b. Relevant exposure – eg drugs, birds, dust?
c. Hx of a CT d/o eg rheumatoid, scleroderma, SLE?
d. Any new assoc sxs – eg athralgias, skin rash, swollen lymph nodes?
e. Impt negatives that allow exclusion of HF or infection – eg hemoptysis, orthopnea, ankle edema, fever?
5. Physical Examination
a. ↑ RR at rest/exercise
b. Cyanosis or ↓ O2 saturation on pulse oximetry
c. Finger clubbing
d. ↓ chest expanstion
e. Fine Velcro-like crackles (most prominent at base of lungs)
f. Restrictive lung volumes on spirometry
6. Ixs
a. CXR +/- HRCT (high resolution CT) → confirm presence of ILD
b. Are findings diagnostic or do you need pathology – eg lung biopsy or bronchoalveolar lavage?
c. Determine severity of dis w lung function and exercise tests
7. Physiology of ILD
a. “Small stiff lungs”
b. ↓ lung vol (VC, TLC)
c. Preserved FEV1/VC ratio
d. Normal airflow at all lung volumes
e. ↓ Diffusion (DLCO)
f. ↓ total lung compliance
g. Widened Aa O2 gradient
h. Respiatory limitation on exercise
8. IPF = Idiopathic pulmonary fibrosis
a. Archetypal ILD
b. Unknown etiology
c. Older pts usu male blue collar workers
d. Characterised by progressive pulmonary fibrosis with median survival <3 yrs
e. Dx made w HRCT in most pts
f. Non-response to treatment – but new drugs hold promise
g. Conventional txs – steroids, cyclophosphamide are ineffective
h. Case Example
i. 57 M
ii. PC – 2 yr hx of ↑ breathlessness + dry cough
iii. Worked as a metal polisher
iv. O/E – clubbed and fine crackles
9. ILDs related to exposure
a. Asbestosis – ILD caused by asbestos, lag time 20 yrs, similar to IPF
b. Pneumoconiosis – coalminers lung, silicosis etc, rare in NZ
c. Histiocytosis X – nodular cystic dis caused by cig smoking, responds to smoking cessation, often seen in younger pts
10. Drugs causing ILD – always take a careful drug and exposure hx in any pt suspected of ILD
a. Amiodarone
b. Nitrofurantoin
c. Chemotherapy (+ radiotherapy) eg bleomycin
d. Immunosuppressants – gold, methotrexate
e. O2 high dose
11. EAA = Extrinsic allergic alveolitis
a. Acute lymphocytic alveolitis and bronchiolitis caused by exposure to inhaled organic antigen
b. Most common in bird fanciers, farmers and horticulturalists – generally older pts
c. Physiology restrictive (and obstructive)
d. Responsive to steroid but pt must avoid ongoing exposure
e. There is a chr form which is similar to IPF where the antigen is not identified
12. Sarcoidosis
a. Mutlisystem granulomatous dis most commonly affecting mediastinal/hilar nodes and lung parenchyma – can involve other tissues eg liver, skin, eyes, heart
b. Dis of younger pts but rare in children
c. Lofgrens syndrome – erythema nodosum, arthralgias, hilar adenopathy (acute form of dis seen in pts of nrth Euro descent)
d. M/PI pts more likely to have extrapulmonary involvement
e. Steroid responsive but not cured by tx
f. Rarely fatal but can cause sig and permanent disability
g. Case Example
i. 26 F
ii. PC – acute onset fatigue, painful rash on legs, aching/swelling of ankles and knees
iii. Abnormal CXR
iv. Presents 2 yrs later with exertional SOB + dry cough
13. Approach to a pt w ILD
a. Establish dx with as much certainty as possible using inter-disciplinary approach (hx/exmn, pathology, radiology
b. If causative exposure applies (eg drug or etal agent) → remove
c. Establish if ILD is responsive to tx and unlikely to regress without
d. Weigh up risk and benefits of tx involving the pt in dec making process
e. Ensure baseline functional and morphological staging eg lung function and exercise tests + CXR/HRCT
f. Undertake regular restaging to monitor response to tx
g. For many ILDs → no proven pharmacologic tx → consider palliative care, transplant OR enrol pts in RCTs of new drugs

LUNG CANCER

1. Intro
a. Most common cause of cancer death in men (and in women in some countries; surpassing breast ca)
b. Major ↑ in women and ↓ in men – reflecting changes in smoking habits over the past 50yrs
c. Types
i. NSCLC (non small cell lung carcinoma) – includes SCC, adenocarcinoma and large cell (undifferentiated) carcinoma
ii. SCLC (small cell lung carcinoma)
2. Etiology
a. Smoking
i. Estimated that smoking causes 80% of lung
ii. 10x ↑ risk of developing lung ca
iii. Clear dose response r/ship - ↑ risk w ↑ quantity of smoking
iv. Risk falls in proportion to number of years after cessation but never completely returns to normal
b. Asbestos
i. Dose response r/ship
ii. 1.5-13 ↑ risk
c. Radon exposure
d. Occupational carcinogens – eg arsenic
e. Nickel exposure
f. Air pollution

Non small cell carcinoma

1. Squamous cell carcinoma (SCC)
i. 30% bronchial carcinomas
ii. >45 yrs
iii. Smokers - strong dose response r/ship with smoking
iv. Slow growing
v. Prognosis related to stage
vi. Most likely associated with cavitation and hypeercalcaemia
vii. Tumour development
1. epithelium of major bronchi develops into squamous metaplasia → dysplasia → Carc in situ → invasive
3. Adenocarcinoma
i. 15-40% of lung ca
ii. ↑ incidence – unknown reasons
iii. In many countries, now more common than SCC
iv. <45 yrs
v. 20% occur in non-smokers (generally female - ?hormone mediated)
vi. More variable presentation and prognosis than SCC
vii. Bronchoalveolar is a distinct clinco pathological entity with variable presentation and beh
viii. Can express aberrant growth receptors – EGFR (epidermal growth factor receptors – response to gefitinib)
4. Large cell carcinoma (undifferentiated)
i. ~15% of cases
ii. Very poor prognosis

Methods of Spread
1. Grows locally – may involve contiguous structures
2. Ultimately invades vascular/lymphatic channels
3. Spread to local lymph nodes
4. Bronchopulmonary nodes (N1)
5. Mediastinal nodes – ipsilateral (N2) and contralateral (N3)
6. Widespread to distant sites – via lymphatic thoracic duct or blood → most freq mets sites = a. bone, b. adrenals, c. liver, d. brain

Clinical Features
1. Depends on location of tumour
2. Loco-regional spread
3. Effect of metastatic spread
4. Paraneoplastic syndrome
5. Sxs tend to be late (asx at early stage)

Presentation
1. Sxs – asx 5-10%
2. Secondary to local endobronchial spread
a. Cough
b. Hemoptysis
c. Wheeze/stridor pneumonitis (2ndry to obstruction)
3. Secondary to peripheral growth
a. Pain – chest or pleural involvement
b. Cough
4. Regional spread
a. Dysphagia (pres on esophagus)
b. Hoarseness (recurrent laryngeal n palsy)
c. Dyspnoea (elevated diaphragm due to phrenic n involvement)
d. Horners syndr (sympathetic chain involvement by pancoast tumor)
e. SVC obstruction and Telangectasia
f. Pericardial tamponade (direct invasion)
5. Metastatic manifestations
a. Fatigue and ↓ activity – 80%
b. Cough
c. Dyspnea
d. ↓ appetite
e. Weight loss
f. Pain
6. Paraneoplastic syndromes
a. Hypercalcemia (ectopic PTH production) - NSCLC
b. SIADH - SCLC

Investigations
1. CXR
2. CT
3. Peripheral tumor
a. Percutaneous FNA – CT or Fluoroscopic guided
b. Bronchoscopy – transbronchail biopsy, brush or needle (fluoroscopic guided)
c. Video assisted thoracoscopy – wedge excision, needle aspiration, thoractomy
4. Central tumor / Unresolving segmental pneumonia / Hemoptysis
a. Sputum cytology
b. Bronchoscopy – biopsy, brush, needle aspiration
c. Percutaneous FNA
d. Thoracotomy

Diagnosis
1. Detailed Hx
a. Smoking hx
b. Exposure to environmental carcinogens
c. F.Hx
d. New sxs – cough, hemoptysis
2. Physical examination
a. Partial or complete airway obstruction
b. Atelectasis or pneumonia
c. Pleural effusion
3. Sputum cytology
a. Require 3x specimens → positive in 60-80% of central tumors but <20% for peripheral tumors
b. SCC > adenocarcinoma
4. Tests
a. CXR – 95% of cases will be abnormal
b. Bronchoscopy + biopsy
c. CT + FNA biopsy

Management of non small cell carcinoma
1. Surgery
a. Only possible way to cure
b. Only 10% of pts operable
c. Stage 1-2 potentially curable by surgery; stage 3-4 are not
2. Prognosis determined by TNM staging
a. Stage 1 >60% 5y survival
b. Stage 2 40%
c. Stage 3 <10-30%
d. Stage 4 <2%
3. Radiotherapy
a. Curative intent for stage 1-2 whom are unfit for surgery
b. All others - palliative
4. Chemotherapy
a. Considered for palliation of unresectable stage 3-4
b. Single agent 15% response rates; ↑ response with combined chemo (30-50%)
c. Median survival ↑ from 4-6 months to 9-12 months
d. No LT survivors
e. ? ↑ survival only a few months but may improve QOL and sx control

Small cell carcinoma

1. Introduction
a. Distinguished from non-small cell because behaves differently
b. 10-20% of lung ca
c. Propensity for developing early mets
d. Smoking = major risk
e. Thought to arise from a different cell
f. Secretes GRP
2. Clinical signs
a. Disseminates to distant organs early
b. 70% have demonstrable metastatic dis → surgery is not an option
3. Staging
a. Limited – tumor confined to one hemithorax and regional lymph nodes that could be encompassed in 1 radiological field
b. Extensive – falls outside above boundary
4. Tx
a. Chemo +/- Radiotherapy
b. Median survival
i. Limited stage → untreated 3 months, treated 12-20 months
ii. Extensive stage → untreated 1 month, treated 7-12 months

Mesothelioma

a. Malignant tumor of the pleura
b. Strong assoc w asbestos exposure
c. No effective tx
d. Median survival 8 months

Hemoptysis

1. Coughing up blood
2. May arise form any part of respiratory tract
3. Distinguish from haematemesis or epistaxis
4. Impt sx that may indicate serious underlying dis → always needs to be investigated
5. Massive hemoptysis (>200 ml) → medical emergency
6. Origin of bleeding
a. Bronchial arteries
b. Pulmonary veins or capillaries
c. Pulmonary arteries or arterioles
d. Abnormal blood vessels
7. Causes of Hemoptysis
a. Neoplasm (endobronchial) → benign, malignant
b. Inflammation / Infection
i. Bronchiectasis
ii. Necrotising pneumonia (includes TB)
c. Cardiopulmonary vascular dis
i. LV failure
ii. PE
iii. Diffuse alveolar hemorrhage syndr
iv. Other – incl mitral stenosis
d. Trauma
e. No cause found

PATHOLOGY OF AIRWAY DISEASE

Bronchial Asthma

Disease characterised by ↑ responsiveness of the tracheobronchial tree to various stimuli
Paroxysmal narrowing of airways occurs, which may reverse spontaneously or with tx
Traditionally 2 main categories
1. Extrinsic or allergic
2. Intrinsic
Pathology
1. Overdistended lungs
2. Mucus plugs
3. Edema of wall – inflammatory infiltrate (often with Eosinophils)
4. Hypertrophy of smooth muscle (severe, chr dis)

Smoking related pulmonary disease

Most pts are smoker and have a mixture of the 3 conditions, but one or other may predominate
1. Emphysema
2. Chronic bronchitis
3. Small airways disease

1. Emphysema
a. Permanent ↑ in size of air spaces distal to terminal bronchiole
b. Destruction of lung tissues
c. Anatomy
i. Acinus = unit of lung tis supported by single terminal bronchiole
ii. Includes terminal bronchiole, several respiratory bronchioles, their alveolar ducts and assoc alveoli
iii. Pulmonary lobule = area lf lung tis outlined by CT septae, measuring1-2 cm and includes several acini (usu 5-10)
d. Pathogenesis
i. Proteases vs antiproteases
ii.
e. Classification
i. Centri vs pan acinar (or lobular)
2. Chronic Bronchitis (mucus hypersecretion)
a. Persistent cough + sputum produnction >3 months in at least 2 consecutive years
b. Other causes of sputum production excl – eg brochiectasis
c. Traditional classification
i. Simple – no physiologic evidence of airflow obstr
ii. Obstructive
d. Pathogenesis
i. Hallmark = hypersecretion of mucus
ii. Large bronchi main site of hypersecretion
1. mucus gland enlargement
2. edema, inflammatory infiltrate
3. Contraction of bronchial smooth muscle
4. blockage of bronchi and bronchioles by exudate
3. Small airways disease
a. General term referring to inflammation/narrowing of airways <2mm diameter (terminal and respiratory bronchioles)
b. Most commonly occurs in smokers along w varying degrees of emphysema and chr bronchitis
c. Pathology – peribronchiolar inflammation + fibrosis, goblet cell metaplasia with mucus plugs
d. Other situations – mineral dust exposure (silica, asbestos), infections etc

Bronchiectasis

Abnormal and irreversible dilation of bronchi which may be generalised or localised
May result in the formation of multiple large spaces or cavities
Most commonly a sequel of bronchiolitis and broncho-pneumonia in c/hood (esp adenovirus)
Other situations – CF, immune deficiencies, cilia abnormalities; localised forms occur distal to bronchial obstruction (eg foreign body)

HYPOXIA

1. Hypoxia definition
a. Lack of O2 – regardless of cause or site
b. Effects occur on a tissue level
c. Acute hypoxia characterised by ↑ cardiac and respiratory rates, mental deterioration +/- cyanosis
d. Hypoxia can present w/o cyanosis
2. 1 kPa = 7.5 mmHg
3. Hypoxia = PAO2 <8 kPa (<60 mmHg)
4. Hypercapnia = PaCO2 <6 kPa (<45 mmHg)
5. Hypoxia and/or Hypercapnia = Respiratory Failure

O2 Cascade

O2 passes from atmosphere to mitochondria down a partial pressure gradient termed the O2 cascade
1. PIO2
a. Influenced by FIO2 and atmospheric pressure
b. 20 kPa (150 mmHg
2. PAO2
a. Influenced by alveolar ventilation and O2 consumption
b. 13 kPa (100 mmHg)
3. PaO2
a. Influenced by venous admixture (V/Q and shunt), gas diffusion and mixed venous O2 content
b. 12.9 kPa (99 mmHg)
4. Tissue capillary PO2
a. Influeced by local O2 delivery and local O2 consumption
b. 12.9-5.3 kPa (99-38 mmHg)
5. Intracellular PO2
a. Low - <2 kPa (<15 mmHg)
b. If intracellular PO2 is abnormally low, this will be due to one of the influences above
c. Intracellular PO2 can be ↑ by ↑ driving pres for the O2 cascade, ie ↑ PIO2 → in practice, this means delivering O2 enriched air to the pt (oxygen therapy)

O2 Therapy

Oxygen is a drug and as such has specific indications for use and side effects
The concentration (not merely the flow rate) and mode of administration to the pt must be charted, and the response to therapy monitored
Methods of delivery
1. Mask
a. Venturi masks use the venturi principle to supply a certain conc of O2 at a specified flow rate (a flow rate other than that specified on the mask must NOT be used)
b. Nasal Prongs - % inspired O2 = 20 + (4x flow rate in l/min) → in practice flow rates above 4 l/min not used
c. Humidified air – Hudson mask + humidifier; machines have been individually calibrated to determine O2 conc delivered by various flow rates; temp seting of 35-37’C
d. Intubation and assisted vent – for advanced respiratory failure; can deliver 21-100% O2
2. O2 should be given to all acutely hypoxic pts eg acute asthma, extensive pneumonia
3. Exception
a. Older pts w severe chr airflow limitation, severe lung dis or problems with control of breathing (eg obesity-hypoventilation syndr) require cautious O2 administration
b. A proportion of such pts have hypercapnia and depend mainly on hypoxic stimulation of peripheral chemo-receptors for respiratory drive
c. High inspired O2 concentrations will abolish this hypoxic respiratory drive and cause hypoventilation and conseq severe acute (on chronic) respiratory acidosis
d. In these pts, initially use low inspired O2 concentrations eg 24,28 or 31%

Pulmonary Function Tests

1. Routine use
a. ABGs
b. Spirometry – FEV1/VC
c. Peak expiratory flow rate
2. Quantitative assessment of pulmonary function is essential in assessment/management of pts w pulm dis
3. FEV1/VC → normal = >70%
4. Tow major types of disease –
a. Obstructive – eg asthma → FEV1/VC ratio ↓
b. Restrictive – eg pulmonary fibrosis → FEV1 and VC ↓ proportionately, FEV1/VC ratio normal or ↑
5. PEFR
a. Wide normal range, but useful for monitoring individual pts w obstructive diseases
b. Not particularly useful for dx nor for determining normality

PLEURAL DISEASE

Objectives
• Physiology + pathophysiology of pleura, pleural fluid t/o and pleural mechanics of pleural disease
• Etiology, Ixs and mgt of pleural effusion
• Etiology and mgt of primary and secondary spontaneous pneumothorax

Pleural Physiology

• Visceral and parietal pleura with space
• Allows movement of lungs relative to chest wall
• But visceral pleura mechanically supports lungs and contributes to inter dependence
• Pleural pressure varies with height and with lung vol
• Mesothelial cells line surface and are source of components of extracellular matrix and chemotactic factors (eg CKs)
• Visceral pleura supplied by bronchial arteries but relatively thick (60 um)
• Parietal pleura (30 um) is a major site of fluid production
• Fluid from systemic blood vessels – Starlings law → leaky pleural membranes → pleural space → to pleural lymphatics via stomas (2-10 um)
• No active t/port of fluid
• Entry of pleural fluid is slow
• Huge reserve for absorption (20-30x before fluid accumulates into pleural effusion)
• Not a passive membrane
• Toll-like receptors bind micro-organisms
• Permeability reduced by VGEF
• Mesothelial cells recruit inflammatory cells (by IL8)
• Facilitate passage of PMNs (ICAMS) and reduce apoptosis (GMCSF)
• Stimulates fibroblast activity and ↓ fibrinolysis

Pleural Effusion

1. Defintion
a. Excessive accumulation of fluid in pleural space
b. Clinical detection possible when >500 ml present
c. Radiological detection possible when >200 ml present (PA CXR) to 50 ml (Lateral CXR)
d. Massive effusions are most commonly malignant in origin
2. Etiology
a. Serous effusions may be transudates or exudates
b. Transudates
i. Occur when bal of hydrostatic forces in the chest favour accumulation of pleural fluid → no ∆ in pleural membr permeability
ii. Occasionally, they may occur bec of mvment of fluid from the peritoneum or retroperitoneal space
iii. Common causes
1. LV failure → ↑ hydrostatic pres
2. Cirrhosis → ↑ hydrostatic pres
3. Hypoalbuminaemia - ↓ oncotic pres
4. Peritoneal dialysis
5. Constrictive pericarditis
6. Nephrotic syndrome - ↓ oncotic pres
c. Exudates
i. Result from pleural and lung inflammation – resulting in a capillary protein leak or from impaired lymphatic drainage of the pleural space → ↑ permeability of pleural membrane
ii. More rarely, effusions consist of blood (hemothorax), pus (empyema) or lymph (chylothorax)
iii. Chylous effusions are caused by leakage of lymph from the thoracic duct due to trauma or infiltration by carcinoma
iv. Common causes
1. Bacterial pneumonia
2. Carcinoma of bronchus
3. Pulmonary infarction (loss of vascular integrity)
4. TB
5. CT dis
3. Clinical features
a. Sxs
i. May be asx (if small)
ii. Breathlessness
iii. Cough
iv. Pleuritic CP
b. Signs
i. ↓ chest wall mvment
ii. stony dull percussion
iii. absent breath sounds
iv. ↓ vocal resonance
v. mediastinum shifted away
4. Ixs
a. CXR
i. Blunting of costophrenic angle or recess (on lateral)
b. Pleural fluid aspiration – unless clinical picture clearly suggests a transudate (eg bilateral, pt w LV failure)
i. Remove for diagnostic purposes and to relieve sxs – don’t insert tube initially
ii. 21G needle and 20 ml syringe
iii. Small effusions often require radiological guidance
iv. Appearance of fluid is noted → bloody, turbid, milky
v. Sample analysis
1. Protein
2. LDH
3. Lights criteria
a. pleural : plasma protein >0.5
b. pleural : plasma LDH >0.6
c. Pleural LDH > 2/3 upper limit of normal for serum
4. pH (<7.3 → suggests bacterial or tumor cell metabolism)
5. Microbial analysis (G stain + culture after inoculating into blood culture bottles, acid-fast bacilli stain and culture)
6. Cytological analysis – differential white cell count, malignant cells
c. Contrast enhanced thoracic CT – if pleural fluid non-diagnostic
i. Pleural fluid still present
ii. Allows for identification of pleural nodulatiry/thickening (malignancy) and image-guided needle biopsy of any focal area of abnormality
d. Pleural biopsy
i. In the absence of any focal areas on CT, a blind percutaneous pleural biopsy can be performed
ii. Tissue is sent for TB smear, culture and histology
5. Management
a. Depends on underlying cause
b. Exudates → drained
c. Transudates → tx of underlying cause
d. Malignant effusions usually reaccumulate after drainage
i. They can be treated by aspiration to dryness followed by instillation into pleural space of a sclerosing agent such as tetracycline or bleomycin

Pneumothorax

1. Definition
a. Presence of air in pleural space
b. May occur spontaneously or be 2ndry to chest trauma
c. Tension pneumothorax
i. Rare unless pt on mechanical ventilator or non-invasive ventilation
ii. In this situation, the pleural tear acts as a one way valve through which air passes only on inspiration
iii. Pos pres builds up → cardiorespiratory function ↓ → eventual cardiac arrest
iv. Tx – immediate decompression by needle thoracentesis; 2nd IC sp – mid-clav line + then intercostals tube drainage
2. Etiology
a. Spontaneous primary pn.thorax (no underlying lung dis)
i. Typically occurs in otherwise healthy tall/thin males aged 25-35 yrs
1. smokers - >90%
2. familial tendency
3. usu at rest or normal activities (not on exertion)
ii. Result of rupture of a subpleural bleb – thought to be a congenital defect in the CT of alveolar wall
b. 2ndry pn.thorax
i. assoc w underlying lung dis – often COPD
1. Obstructive – COPD, CF
2. Restrictive – histiocytosis X, PLAM
3. Cavitory – bullous emphysema, necrotising pn
4. Traumatic – includes iatrogenic
3. Pathophysiology
a. Loss of negative intra-pleural pres
b. ↓ VC
c. ↓ PaO2 → low V/Q, shunt
4. Clinical Features
a. Sxs
i. Sudden onset pleuritic CP (stabbing like pain)
ii. ↑ breathlessness
b. Signs
i. ↓ chest expansion
ii. ↓ breath sounds
iii. hyper-resonance
iv. Tension pn.thorax signs
1. distress
2. tachycardia and tachypnea (due to hypoxia and ↓ CO)
3. shift of mediastinum to opposite side (absent breath sounds on affected side)
4.
5. Investigations
a. CXR – standard PA
i. Size of pn.thorax estimated by measuring the dist from the lat edge of the lung to the inner wall of the ribs
ii. >2cm implies pn.thorax is at least 50% (large) – sml vs large classification
iii. May be a shift of trachea and mediastinum assoc w a large pn.thorax
iv. PTX vs Bulla (see diagram)
1. bullous epnysema – severe respiratory compromise, do not place chest tube
b. Lateral decubitus film – provides additional info when pn.thorax suspected but not confirmed by standard films
c. CT Scan
i. To differentiate severe bullous lung dis from pn.thoraces and save the pt a potentially dangerous needle aspiration
6. Management
a. Depends on evidence of tension/resp failure, sxs, underlying lung dis, size of PTX, social circumstances
b. Observation + supplemental O2
i. 4x ↑ absorption rate
ii. underused
iii. consider if no underlying lung dis, small (<2cm rim) or not SOB, and if social circumstances allow it
iv. f-up at 48 hrs or if worsens
v. resolves at 1.25% p/day
c. Aspiration
i. More rapid resolution
ii. Not for 2’ PTX (ie underlying lung dis)
iii. Size not a contra-indication
iv. Technique not w/o complications
d. Insertion of ICT (intercostal tube)
i. If underlying lung dis – ie 2’ PTX
ii. Technical competence essential
iii. Attach to UWSD? – suction ?after 24 hrs
iv. Allows rapid re-expansion
v. Do NOT clamp tubes hen bubbling or during transfer
vi. Do not advance tubes after insertion
e. Spontaneous primary pn.thorax
i. High flow O2 (10 l/min)
ii. If no breathlessness or <2m on CXR → consider d/c + return if breathlessness
iii. Otherwise → aspiration (2 attempts) → if successful, then consider d/c
iv. If unsuccessful → intercostals drain
v. Ø smoking → ↓ recurrence rate
f. 2ndry pn.thorax
i. all pts should remain in hospital
ii. a single attempt at aspiration is recommended only in minimally breathless pts <50y w small pn.thoraces
iii. Chest drain insertion in all other pts
iv. O2 via fixed performance mask to pts w COPD

7. Complications – of PTX and Management
a. Failure of lung to re-inflate
i. Ongoing air leak
ii. ↓ lung compliance
iii. endobronchial obstr
iv. blocked/misplaced tube
b. Subcut emphysema
c. Hemothorax
d. Pain
e. Re-expansion p.edema
8. Indications for referral to respiratory physician
a. Persistent air leaks – >2 days
b. Failure of lung to re-expand - >1 day
c. Worsening subcut emphysema
d. Re-expansion p.edema
e. Devt of pl.effusion
f. Recurrent or bilateral PTX
9. Recurrent rates
a. Same side – 20% after 1, 40% after 2, 80% after 3 (or 50% at 4 yrs)
b. Opposite side – 10-20%
c. Recurrence greatest in subseq few months
d. More likely to recur if smoke and have subpleural blebs
e. Avoid scuba diving and sky diving

PNEUMONIA

1. Definition
a. Acute respiratory illness assoc w recently developed radiological pulmonary shadowing which may be segmental, lobar or multilobar
2. Etiologic Classification (preferred)
a. Community acquired (CAP)
b. Hospital acquired (nosocomial) – often post-op
c. Pneumonia in the immunosuppressed or pts w underlying lung damage
d. Aspiration pneumonia
3. Traditional Classification
a. Lobar pneumonia
i. Radiological and pathological term referring to homogenous consolidation of one or more lung lobes (often assoc w pleural inflammation)
ii. Organism - pneumococcus usually
iii. Characteristics – intra-alveolar exudates → consolidation (amy involve entire lung)
b. Bronchopneumonia
i. Patchy alveolar consolidation associated w bronchial and bronchiolar inflammation affecting both lower lobes
ii. Organisms – S.aureus, Klebsiella
iii. Characteristics – acute inflammatory infiltrates from bronchioles → adjacent alveoli, patchy distribution involving one or more lobes
c. Atypical (interstitial) pneumonia
i. Organisms – virus, mycoplasma, legionella, Chlamydia
ii. Characteristics – diffuse patchy inflammation, localised to interstitial areas, alveolar walls, distribtution to one or more lungs
4. Pathophysiology
a. Alveoli inflammation and fluid accumulation
b. Caused by bacteria, viruses, fungi, parasites, chemical or physical injury
5. Presentation
a. Cough
b. CP
c. Fever
d. Dyspnea
6. Complications
a. Respiratory failure (ARDS)
i. Infection and inflammation → lungs fill with fluid and become stiff → O2 extraction difficulties → required mechanical vent
b. Sepsis/Shock
i. Bacteraemia (esp S.pneumoniae) → immune response (incl cytokine secr) → required IV fluids to ↑ BP
c. Pleural effusion
i. Empyema (pus in body cavity) occurs when micro-organisms enter pleural cavity
ii. Thoracentesis = removal of pleural fluids → analysis; chest tube may be reqd
1. Transudate - ↓ protein content – CHF, nephritic syndrome, hepatic cirrhosis
2. Exudate - ↑ protein content – malignancy, pneumonia, trauma
d. Lung abscess
i. Bacteria form a pocket of infected fluid (typically with aspiration pneumonia)
ii. Abscess seen best on CXR or CT
iii. A/Bs usu adequate but surgical draining sometimes reqd
iv. Predisposing factors – bronchial obstruction (eg ca), aspiration of gastric contents (esp alcoholics, epileptics – LOC)
7. Prognosis
a. Tx – usu cured within 1-2 wks (viral pn may last longer)
b. Bacterial pn – 5% die (depends on how ill person is when first diagnosed)
c. Septicaemic pts – 20% mortality

1. CAP

1. Epidemiology
a. 0.5-1% of adults pa (mostly young and old)
2. Risk Factors
a. Smoking
b. URTIs
c. Alcohol
d. Corticosteroid therapy
e. Old or young age
f. Recent flu inf
g. Pre-existing lung dis
3. Etiology
a. Streptococcal pneumoniae (pneumococcus) – winter, all age groups, rapid onset, high fever, pleuritic cp, rusty sputum
b. Mycoplasma pneumoniae (young adults)
c. Chlamydia pneumoniae (young adults)
d. Haemophilus influenzae (usu elderly or those w chr lung dis)
e. Legionella penumophilia (elderly, foreign travel, local epidemics)
4. Presentation
a. Acute illness with systemic features – fevers, rigors, shivering, vomiting, loss of apetite
b. Cough
i. Initially painful and dry
ii. Later - expectoration and mucupurulent sputum
c. Pleuritic CP
d. Headache common
e. Rusty sputum → S.pneumoniae
f. Hemoptysis - uncommon
5. Ixs
a. Bloods – wcc elev, CRP elev
b. CXR – infiltrate on CXR not always pneumonia
c. Gas exchange assessment → pulse oximetry, ABG if O2 sat <92% or if pn severe
d. Sputum culture → microbial dx + A/B sensitivity – only necessary in severe cases; sens/specf of testing poor, specific organism in <50%
e. Clinical, radiological and lab ixs → do NOT allow reliable identification of pathogen in individual cases
6. Risk Stratification –
a. CURB Score → determines mortality risk and guides admission to ICU
i. Confusion
ii. Urea >7 mmol/l
iii. RR >30
iv. BP <90/<60
v. 65+ yrs
b. 1x point for each – scores → 0-1 home tx / 2 consider hospitilsation / 3+ severe pn, hosp reqd
7. Differential Dx
a. Pulmonary infarction
b. TB
c. Pulm edema (can be unilateral)
d. Malignancy
8. Management
a. Rest
b. Ø smoking
c. O2 and fluids → aim O2 sat >90%
d. A/Bs – generally best guess as organism unknown, don’t delay, don’t change A/Bs in first 72 hrs (lack of response probably not due to A/B choice but more likely the devt of a complication (eg empyema) or presence of underlying dis (eg endobronchial obstruction)
i. Uncomplicated CAP
1. Amoxicillin 500 mg Q8H PO
2. Erythromycin 500 mg Q6H PO
ii. Severe CAP
1. Erythromycin 500 mg Q6H IV + Co-amoxiclav 1.2 g Q8H IV
iii. Suspeted mycoplasma/legionella → Erythromycin + Rifampicin in severe cases
iv. Drug Resistant pneumococcus → flouroquinolones (moxifloxacin, sparfloxacin)
e. Analgesia for CP – care with opiates due to respiratory depression
f. Phsyiotherapy – to remove secretions
g. Bronchodilators
h. Repeat x-ray at 6-8 wks (or 4 wks if young and no co-morbidities) → takes this long to clear up
9. Delayed recovery suggests -
i. complication (empyema)
ii. incorrect dx
iii. 2ndry to bronchial obstruction
iv. recurrent aspiration
10. Prognosis
a. <5% mortality
b. 25% mortality if hosp reqd
c. 40% mortality if ICU reqd

Tx Protocols
1. CAP – outpatient w/o comorbidities (pneumococcus > mycopl/leg/chlam – macrolide, doxy, amox, co-amoxyclav)
2. CAP – outpatient w comorbidities (pneumococcus > H.influenzae > S.aureus – amox, augmentin, macrolide, doxy)
3. CAP – inpatient w/o comorbidities (pneumococ > h.influ – IV b-lactam +/- macrolide/doxy, anti-pneumococcal fluoroquinalone)
4. CAP – inpatient w comorbidities – as above
5. CAP – icu admis (pneumococcus > legionella > h.influ > s.aurues – IV B-lactam (cefotaxime + IV macrolide or IV fluoroquinalone)

2. Hospital acqd pneumonia (nosocomial pn)

1. Definition
a. New episode of pneumonia occurring >2 days after hospital admission
b. Includes post-op pn, certain forms of aspiration pn and pneumonia/bronchopneumonia developing in pts w chr lung dis, general debility or those on assisted vent
2. Epidemiology
a. 22-5% of all hospital admissions
b. Esp elderly
3. Predisposing Factors
a. ↓ host defences
i. ↓ immunity – eg. corticosteroid tx, DM, malignancy
ii. ↓ cough reflex - eg. post op
iii. ↓ mucociliary clearance – eg. anaesthetic agents
b. Aspiration of nasopharyngeal or gastric secretions
i. Immobility or ↓ consciousness
ii. Vomiting
iii. NGT
c. Bacteria introduced into LRT
i. ETT, tracheostomy
ii. Infected ventiliators/nebulisers
d. Bacteriaemia
i. Abdominal sepsis
ii. IV cannula infection
4. Organisms
a. Escherichia
b. Pseudomonas
c. Klebsiella
d. S.aureus (incl MRSA)
e. Anaerobes
5. Clinical Features
a. Similar to CAP
b. Elderly/debilitated pt developing acute bronchitis sxs followed by ↑ cough, sputum purulence, fever (over 2-3/7)
c. Dyspnea
d. Central cyanosis
e. Signs - crackles
6. Investigations
a. FBC – neutrophil leucocytosis
b. CXR – mottled opacities in both lung fields (esp lower zones)
7. Management
a. A/B G- Cover → 3rd gen cephalosporin (cefotaxime) + aminoglycoside (gentamicin)
b. Physiotherapy
8. Prognosis
a. Mortality – 30% (high)

Aspiration Pneumonia, Lung Abscess, Empyema

1. Pathophysiology
a. Aspiration of oro-pharyngeal contents → aspiration pn (necrotizing infection) → lung abscess (necrosis + coalescence) → para-pneumonic effusion/empyema (pleural leaks)
b. Risks of aspiration - ↓ LOC, impaired cough
i. General anaesthesia
ii. Excess alcohol/drugs
iii. Head injury
iv. CVA
v. Seizures
vi. Coma
vii. High microbial load

Lung Abscess
1. Definition
a. Localised area of destr of lung parenchyma in which infection by a pyogenic organism results in tissue necrosis + suppuration
b. Often caused by aspiration – esp during altered consciousness (alcohol most common condition predisposing to lung abscess)
2. Organisms
a. Mixed
b. Anaerobes (predominately) → eg. Bacteroides
3. Presentation
a. Hx of aspiration (not always; may also be insidious and delayed)
b. General sxs → lassitude, anorexia, weight loss
c. Productive cough
d. Fever
e. Sweats
f. Dyspnea
g. CP
h. Hemoptysis
4. Radiology
a. CXR – parenchymal infiltrate, one or more areas of homozygous density in which air-fluid levels develop
5. Management
a. Must include anaerobic cover
b. Aspiration pn → Co-amoxiclav 1.2 g Q8H + Metronidazole 500 mg Q8H

Empyema
1. Definition
a. Pus within a natural body cavity
b. Differentiated from an abscess in which a collection of pus occurs in a newly formed capsule as opposed to a pre-existing cavity
c. Pleural space commonly affected → pyothorax (usually due to pneumonia)
2. Organisms
a. Mixed anaerobes 80%
3. 3x Stages
a. Exudative → accumulation of pus
b. Fibrinopurulent → loculation of pleural fluid (creation of grape like pus pockets)
c. Organising → potential for lung entrapment by scarring → pulmonary fibrosis → eventual cor pulmonale
4. Presentation
a. Fever
b. Chest pain
c. Cough
d. Sweating
e. Dyspnea
5. Physical examination
a. Clubbing
b. Dull percussion
c. ↓ breath sounds
6. Investigations
a. CXR → pleural effusion
b. U/S → confirms size + location of pus pocket and presence of fibrin aggregates
c. Thoracentesis → confirms dx
7. Management
a. Avoid delays → prevent progression to organizing phase
b. ICT = Intercostal tuble / chest tube → inserted to drain pus from pleural space
c. A/Bs IV – Co-amoxyclav 1.2 g Q8H + Metronidazole 500 mg Q8H (as per lung abscess) → 4-6 wks
d. Surgery – if med tx fails (ie persisting sepsis despite ICT etc)

SLEEP DISORDERS AND SLEEP-DISORDERED BREATHING

Background on Human Sleep

1. Function
a. Not clearly understood
b. Restorative – abolishes both sleepiness and fatigue
2. Requirements
a. Individual – varies 4-10 hrs
b. Most people feel best after 7-8 hrs
c. Total sleep deprivation in any animal → death in 2-3 wks
3. Structure of sleep
a. 5 stages based on EEG (electroencephalogram)
b. Cycle through each sleep stage in cycles lasting ~90 mins (4-5 cycles per night)
c. The proportions of each stage changes as the night progresses
d. Sleep stages
i. Stage 1 – light sleep
1. first few mins
2. lasting only a few mins
3. 2-5% of night in this stage
4. Can be difficult to distinguish from wakefulness
ii. Stage 2 – sleep
1. sleep spindles and k-complexes on EEG
2. 25-30% of night
3. ↑ proportion of stage 11 sleep with each successive sleep cycle during the night
iii. Stage 3 – slow wave initiation
1. slow waves with large amplitudes begin to dominate the EEG
2. first stage of slow wave sleep
3. usu a precursor of stage 4 (in older subjects, only stage 3 may be seen)
iv. Stage 4 – well established slow wave sleep
1. arousal thresholds are low2. amount is huge in children, falling to 30% in adults, then fades in late middle age
3. totally absent in many elderly subjects, esp men
v. Stage 5 – REM sleep
1. v fast EEG frequencies with profound loss of muscle tone
2. eye mvments may come in phases
3. most if not all dreaming occurs in this phase
4. brain v metabolically active with high O2 consumption
5. young adults – 15-25% of sleep
vi. Note - sleep entered through stage 1 in adults but young children and narcoleptics enter via REM
e. During sleep – skeletal mus tone ↓ to a varying extent, the most profound hypotonia occurring in REM (exception is the muscles of respiration)
f. Autonomic tone changes during sleep → ↓ HR, ↓ BP, ↓ RR and depth
i. During REM sleep → autonomic instability with wild swings in HR, BP, RR and freq

Common sleep complaints

EDS = Excessive daytime sleepiness
1. Sleepiness is the subjective sensation of the need to fall asleep
2. To stay awake, a person has to fight sleep bec the sleep promotion is strong
3. Most apparent when the individual is unstimulated eg relaxing watching tv or driving in monotonous conditions
4. Different from fatigue which is more of a physical sensation
5. Assessing daytime sleepiness
a. Questionnaires – limitations esp as individual may not have insight into how sleepy they are
b. Epworth sleepiness score
i. 8 situations, scored 0-3 leading to a score of 24
ii. 0 = no chance of falling asleep, 1 = slight chance, 2 = moderate chance, 3 = high chance
c. MSLT = multiple sleep latency test
d. MWT = maintenance of wakefulness test
6. Concept of sleep hygiene
a. To maximise sleep quality + quantity, many factors are involved incl –
i. Sleeping at regular hours
ii. Comfortable sleeping evt
iii. Clear influence of habits surrounding going to bed

Disorders of Initiation and maintenance of Sleep

1. Insomnia
a. Definition
i. Perception by the sufferer that sleep is inadequate, usu in quantity, often in quality
ii. Most complain of difficulty initiating sleep or repeated awakenings followed by difficulties reinitiating sleep
b. Types
i. Acute insomnia
1. <3 wks duration
2. Very common esp with acute life crisis eg exams, grief reactions etc
3. usu self limiting but may become chr if triggering experience profound or prolonged
ii. Chronic insomnia
1. >3 wks
2. Primary
a. Assoc w Type A personalities – “take the day to bed with them”
b. Possible hx of mental illness
c. Primary aim of therapy – to help cope with the problem and diffuse anxieties about sleep and impact on their life
3. Secondary
a. Triggered or assoc w either –
i. Physical illness – one that may directly disturb sleep (eg pain syndromes, noctura) or can be more subtle (eg LF leads to sleep inversion ?altering clearance of hormones related to sleep regulation)
ii. Mental illness – eg depr (assoc w early morning wakening)
2. Narcolepsy
a. Rare genetic condtions – 0.1% of Caucasian popns
b. ?deficiency of hypocretin secreting cells in brainstem
c. Hypersomnolence + attacks of overwhelming need to sleep beyond individual’s control
d. Represent an attempt by REM sleep to push into wakefulness
e. Individual experiences hallucinations at sleep onset where dreaming starts while pt is awake
f. Note – sleep paralysis or hallucinations occur on wakening due to profound muscle hypotonia of REM persisting into wakefulness
g. 70+ % suffer from cataplexy (emotional stimulus eg laugh, fright) lead to REM hypotnia → range from involuntary closing of eyes to total collapse (mistaken for epilepsy!)
h. Dx – multiple sleep latency test – demonstrates excessive sleepiness + sleep onset REM
i. Tx – difficult, regular daytime naps, stimulants (amphetamine based) and TCAs to suppress REM sleep
3. Periodic limb movement d/o
a. Rhythmical twitches of limbs during sleep (similar to myotonic jerk everyone sometimes experiences when falling asleep)
b. Occurs every 10-15 secs
c. Usu involve legs
d. Often incidental finding on sleep studies or referral due to partner disturbance
e. In a minority – will cause recurrent wakening or EDS due to fragmentation of sleep
f. Dx – sleep study, freq and impact of jerks on sleep + clinical picture + sxs
g. Tx – difficult, sedative drugs (eg clonazepam; but this will make any co-existing sleep disordered breathing worse), mvment d/o drugs (eg carbidopa), success rates vary, pt committed to lifelong therapy
4. D/os of Circadian rhythm
a. Occurs when the internal clock (which controls the propensity to sleep + quality of sleep and is influenced by circadian hormonal variations) is out of phase with the day night cycle
b. Major influences on internal clocks are – light/dark cycles, food intake, activity patterns
c. Normal human clock averages 25.5 hours but the stimulus of light/dark forces it to 24 hrs
d. Irregular hours and lifestyle (esp if meal and sleep times are disjointed) can lead to internal clock confusion
e. Most clocks reset quickly when given enough cues, however in some, the clock may have difficulty being retrained back into a normal cycle leading to night owls who cant sleep till 3am then have to wake at 6am → become chronically sleep deprived
f. Sleep workers may never be able to resume a refreshing + restorative sleep pattern after leaving shift work → may be the reason for higher morbidity from both physical and mental illness
g. Dx – detailed hx, sleep diary may be reqd to determine sleep/exercise/eating patterns, sleep studies of limited value
h. Tx – difficult, ↑ stimuli for normal sleep such as early morning brightness + regular eating may be sufficient
i. Bright light therapy with bright lights like strong x-ray boxes at set times of day and advancing those times successively can recapture sleep/wake cycle and lead it back to normal pattern
ii. Pts may need this at regular intervals, as often relapse after a few weeks

Sleep disordered breathing

1. Physiology
a. During sleep – chemoreceptors are reset, minute vent drops, O2 consumption ↓
b. Change in posture altering functional residual capacity and respiratory mechanics
c. Progressive hypotonia of deepening sleep affects accessory muscles of respiration → intercostal muscles and some muscles of the upper airway
d. As we breathe by sucking air in, the resultant floppiness of the throat causes a variable degree of narrowing (↑ resistance) depending on the initial size + shape of the throat, age, and presence of any obstructions (eg deviated septum , residual tonsillar hypertrophy etc)
e. The result is ↑ load on the diaphragm (major respiratory mus during REM)
f. This load can become intolerable if there is severe upper a/w narrowing combined with obesity leading to frank respiratory failure
g. Alternatively, the upper airway may be sucked shut and obstruct, effectively strangling the sufferer (asphyxia) and causing apnea, which then triggers arousal from sleep
h. Arousals are potentially dangerous as they are accompanied by sympatho-adrenal response → dramatic ↑ in BP and HR
2. Terminology
a. Apnoeas – pauses in breathing, occur in sleep, usu brief but prolonged apneas (>10secs) are potentially pathological
b. Hypopneas – shallowing breaths, much variation and debate about how to measure them and what point they become clinically sig
c. RERA (respiratory related arousal) – variations in breathing that may not look very impressive but are sufficient to cause an arousal and sleep fragmentation; usu recognised by a change in the shape of the airflow signal, flattening suggesting airflow limitation or paradoxical mvment betw thorax and abdomen during breathing cycle
d. RDI (respiratory disturbance index) – number of apneas + hypopneas + RERA per hour
3. Snoring and obstructive sleep apnea
a. Snoring – common, indicates narrowing of upper airway sufficient to cause turbulence with resultant vibration of the upper a/w walls and soft palate
b. 40% of middle aged men (20% women) snore regularly
c. obesity = ↑ snoring risk (? Upper a/w narrowing, ∆ in shape)
4. Simple snoring
a. Loud regular snoring
b. Often in all positions
c. No evidence of sleep disruption
d. Ø assoc sleepiness
5. UARS (upper airway resistance syndr)
a. Controversial topic
b. Some loud snorers are very sleepy but have no apnoeas or hypopneas
c. In some such pts, measuring respiratory effort via balloon in esophagus demonstrates ↑ respiratory effort being reqd to maintain airflow and avoid apnea or hypopnea
d. Such respiratory effort can then cause arousal and sleep disruption
e. If flow is the same but effort has ↑, then clearly the resis of the a/w must have ↑
6. OSA (obstructive sleep apnea) or SAHS (Obstructive sleep apnea/hypopnea syndr)
a. Defintion
i. Apneas or hypopneas due to upper a/w narrowing or full obstruction leading to clinical sxs
ii. Episodes disrupt sleep leading to EDS
iii. Extent of daytime sleepiness does not correlate well with severity as different individuals differ in their resis to sleep disruption
iv. If prolonged or if sufferer has cardio-resp dis, then O2 sat ↓ and profound desat may be seen
v. The micro-arousals can be hard to detect on EEG
b. Epidemiology
i. Common – 2-4% of middle aged men, 1-2% of females have some degree of OSA– in USA
ii. M/PI may be at ↑ risk due to facial shape
c. Risk Factors
i. Shape of throat (2ndry to facial shape eg retrognathia)
ii. BMI – neck fat; it is not clear why some overweight individuals develop OSA and others dont
iii. Age - ↑ collapsibility of throat with age
iv. Male - ?testosterone related
v. Variety of medical conditions that alter the upper airway eg myxoedema, acromegaly
d. Presentation
i. Pts c/o of sleepiness
ii. Difficulty in concentration and memory
iii.
e. Treatment
i. Weight loss – extent unpredictable as some will have congenitally narrow throat
ii. Positional tx – keep subject off back (if sleep studies show OSA largely when supine)
iii. CPAP – continuous pos a/w pres
1. only reliable proven tx for OSA
2. pos pres applied to upper a/w via a self sealing nasal mask
3. this splints open the upper a/w during sleep preventing narrowing
4. not a cure
5. does improve QOL, daytime sleepiness, psychometric function (reaction times, mem etc)
6. 10-15% cant use this therapy for a variety of reasons eg claustrophobia from mask
iv. Surgery
1. largely used as a tx for simple snoring, even then a limited success rate
2. totally rebuilding the lower face and advancing the maxilla and mandible can be v successful in subjects w small or retrognathic jaws
3. complex surgery – rarely used in pts w a normal facial shape
v. Mandibular advancement
1. mandibular advancement devices are dental devices worn at night
2. these attempt to hold the tongue forward (snorguard) or pull forward the jaw (snorex)
3. many designs
4. can occasionally be v successful, however largely used in tx of snoring or mild OSA only
f. Complications
i. OSA → RF for HTN (even with relatively infrequent apneas/hypopneas (2-5x p/hr)
1. mechanism not fully understood but repeated arousals → sym stim → appears that interactions betw recurrent asphyxia + desaturations interact w sym stim → autonomic dysfunction, abnormal control of BP + possibly LT cv damage w ↑ risk of strokes and MI
7. Central Apnea and Hypoventilation
a. Failure to breathe during sleep, not due to a/w obstr but due to failure in drive to breath
b. 2 forms
i. Trigger Failure
1. most common form not a dis as we all have brief central apneas in sleep assoc w mvment or during transits betw sleep stages
2. these pauses are often only ever noticed in snorers leading to referral for possible OSA
3. Extreme form of central apnea is odin’s course where a baby is born w no central drive to breathe (they have a respiratory arrest whenever they fall asleep)
4. In adults, central apneas most commonly seen in severe HF w resultant cheynes stokes respiration (also caused by variety of drugs) - waxing and waning of resp w TV progressively ↓ until apnea followed by restart of breathing building up to a crescendo w v large breaths which may cause arousal due to assoc resp effort
ii. Nocturnal Hypoventilation
1. many etiologies – incl brain damage
2. remember – we all hypoventilate in sleep there is ↓ respiratory drive
3. not a problem if you have normal lungs but in severe respiratory disease, then ventilatory muscles that can only just cope during the day get less stimulus and vent may be inadequate → hypoventilation with hypoxia (desaturation) and hypercapnia
4. thus, any pt w a low PaO2 when awake (<8 kPa and O2 sat 92%) will desaturate at night in sleep
8. Disorders of alertness and sleep promotions
a. Rare
b. Daytime somnolence yet sleep normally and have no disruption to sleep or sleep disordered breathing
c. “idiopathic hypersomnolence”
d. some have poor sleep quality and may have a hx of drug/alcohol abuse, toxin exposure or major brain injury

VENOUS THROMBOEMBOLISM (VTE)

1. Risk Factors - Thromboembolism
a. Venous stasis – eg travel, immobilisation, pregnancy
b. Trauma – esp to lower limbs
c. Pro-coagulant states
d. ↑ age
e. Malignancy
f. Virchow’s triad – encompasses three broad categories of factors thought to contribute to venous thrombosis
i. Alterations to blood flow (stasis)
ii. Injury to vascular endothelium
iii. Alterations in the constitution of blood (hypercoagulability)
2. Results in thrombus formation in a deep vein with risk of embolus to the pulmonary arteries
3. DVT
a. Presentation of DVT
i. Swollen tender calf or thigh
ii. Hx of risk factors – eg overseas travel or recent injury/surgery
b. Differential Dx
i. Ruptured bakers cyst
ii. Cellulitis
c. Ixs
i. Doppler U/S → reduced venous flow in deep venous sys (confirms dx)
ii. D-dimer
1. Product of fibrin degradation
2. High negative predictive valve – but many false positives (↑ w age)
3. Correlates w size of thrombus
4. Useful for screening but not proving VTE
d. Tx - DVT
i. Below knee → compression bandage unless symptomatic → v low risk of embolus
ii. Above knee → anticoagulation for minimum 3/12 (longer if residual thrombus)
4. Pulmonary Embolism
a. Defintion
i. Complication of deep vein thrombosis (DVT) which may or may not be symptomatic
ii. Occurs in 30% of pts w DVT
iii. True incidence unknown
iv. Over diagnosed in the young and under diagnosed in the elderly
v. Common medical problem
b. Pathophysiology
i. Large embolus can obstruct a large pulmonary artery → distal pulmonary infarction
ii. Result in hemodynamic changes
1. Pulm HTN
2. ↑ RV filling pres
3. ↓ LV filling → systemic hypotension
4. Worsening R heart oxygenation + eventually failure
iii. It will also cause hypoxaemia due to V/Q mismatch
iv. Death in ~10% (usually sudden)
c. Presentation of PE
i. Sxs
1. Acute onset dyspnea
2. CP
3. Syncope
4. Hemoptysis
ii. More common in older pts but sxs less dramatic
iii. Always consider in a pt w ca
iv. Signs
1. Non-specific
2. Tachypnea
3. Tachycardia
4. Hypotension
5. Plerual rub
d. Immediate Ixs
i. Hypoxia
ii. ECG or CXR changes
iii. V/Q Scan
1. Helpful if normal or strongly positive – not in the case in 80%
2. Result expressed as a probability
3. Unsuitable for pts w pre-existing lung dis (many)
iv. CT pulmonary angiogram (gold standard)
1. Previously gold standard was pulmonary angiography
2. CT pulm angiography considered equivalent but with greater access and pt comfort
3. Allows visualisation of lung parenchyma and info about other dxs
4.
v. Radiological dx is necessary for dx of PE
e. Differential Dx
i. HF
ii. MI
iii. Pneumonia
f. Approach to the pt w a suspected PE
i. Are s/s + initial tests suggestive and pt is at risk? → if yes, proceed to d-dimer
ii. If d-dimer negative → stop and consider other dxs
iii. Are you going to tx the pt for a PE → if yes, proceed to CTPA
iv. If pt hypotensive or hypoxaemic → stabilise prior to CT
v. If CTPA negative → withhold tx for PE and consider other dxs
g. Tx - PE
i. Resus – O2, inotropes, fluid
ii. Anticoagulation – heparin then warfarin
1. IV heparin bolus + subsequent infusion → APPT monitoring
a. Note – heparin can be given with thrombolysis
2. OR daily subcut LMWH → no monitoring reqd
3. Start oral warfarin soon after commencing heparin
a. 5-10mg daily
b. Monitor INR (aim 2.5)
c. Continue 3-6/12
4. Complications of anticoagulation
a. Bleeding
b. Drug interactions with warfarin
c. Teratogenicity with warfarin
d. Heparin induced thrombocytopenia
e. Heparin induced osteopenia
5. a
iii. If massive PE → consider rTPA (thrombolysis) or surgery (pulmonary endarterectomy)
iv. If pt compromised and DVT present or recurrent PE while adequately anticoagulated → consider IVC filter
h. Subsequent Management
i. Explore risk factors and mitigate – eg estrogens, immobility
ii. Ensure complete resolution of thrombus – consider repeat imaging at 6-12 wks
iii. If large PE – ensure no persisting pulm HTN
iv. Ensure pt aware of risk of subsequent VTE
5. Prevention of VTE
a. High risk pts → LMW heparin prophylaxis (place of aspirin uncertain)
b. Travellers → ?aspirin
c. Recurrent VTE – depends on risk/benefit

SUMMARY - RESPIRATORY

Pneumonia

1. Def – acute resp illness caused by bacteria, viruses etc involving alveolar inflammation and fluid accumulation
2. Etiologic classification (preferred) – a. CAP, b. Hospital acqd (nosocomial), c. pn in the immunocompr, d. aspiration pn
3. Traditional classification
a. Lobar pn – homogenous consol of 1 or more lung lobes, usu pneumococcus, often assoc w pleural inflame
b. Bronchopneumonia – patchy alveolar consol w bronchial/bronchiolar inflam, affecting both lower lobes, often S.aureus, klebsiella
c. Atypical (interstitial) pn – diffuse patchy inflammation, localised to interstitial areas and alveolar walls, typically viral, mycoplasma, legionella, chlamydia
4. Presentation
a. Cough
b. CP
c. Fever
d. Dyspnoea
5. Complications
a. Respiratory failure (ARDS) – infection/inflammation, O2 extraction difficulties, mech vent reqd
b. Sepsis/Shock – bacteraemia esp from s.pneumoniae, immune response
c. Pleural effusion + potential empyema – micro-organisms + suppuration in pl. cavity, thoracentesis (pl fluid drain) reqd
d. Lung abscess – esp from aspiration pn

CAP
1. Epidem – 0.5-1% adults pa
2. RFs – smoking, URTIs, alcohol, corticosteroid tx, old/young, pre-existing lung dis
3. Etiology
a. S.pneumoniae (pneumococcus) – winter, all age grps, rapid onset, high fever, pleuritic cp, rusty sputum
b. Mycoplasma pneumoniae and Chlamydia pneumoniae – young adults
c. Haemophilus influenzae – usu elderly or those w chr lung dis
d. Legionella pneumophilia – elderly, foreign travel, local epidemics
4. Presentation
a. Systemic feats – fevers, rigors, vomiting, appetite loss
b. Cough – initially painful and dry, later expectoration and mucopurulent sputum
c. CP – pleuritic
d. Rusty sputum (S.pneumonaie)
e. Headache common
f. Hemoptysis uncommon
5. Ixs
a. Bloods – wcc elev, CRP elev
b. CXR infiltrate
c. Gas exchange assessment – pulse ox, ABG if O2 sat <92% or severe pn
d. Sputum culture – only reqd in severe cases, specific organism identified in <50%
6. Risk stratification – CURB Score (one point each, 0-1 = home tx, 2 = consider hosp, 3+ = severe pn, hosp reqd)
a. Confusion
b. Urea >7 mmol/L
c. RR >30
d. BP <90/<60
e. 65+ yrs
7. Differentials
a. TB
b. Pulmonary edema
c. Malignancy
d. PE
8. Management
a. Rest
b. Stop smoking
c. O2, IVF
d. A/Bs (don’t delay, best guess)
i. Uncomplicated CAP – a. Amoxicillin 500 mg Q8H, or b. Erythromycin 500 mg Q6H PO
ii. Severe CAP – Co-amoxy 1.2 g Q8H IV + Erythromycin 500 mg Q6H IV
iii. Suspected mycoplasma/legionella – Erythromycin
iv. Drug resistant pneumococcus – fluoroquinolones (eg moxifloxacin)
e. Analgesia
f. Physiotherapy
g. Bronchodilators
h. Repeat x-rays at 6-8 wks (4 wks if young + no-comorbidities)
9. Delayed recovery – suggests complication eg empyema, bronchial obstruction, recurrent aspiration
10. Prognosis - <5% mortality, 25% if hosp reqd, 40% if ICU reqd

Hospital acquired pneumonia
1. Def – new episode of pn, >2 days after adm (includes post-op pn and aspiration pn)
2. Epidem – elderly
3. Predisposing factors –
a. decr host defences – decr immunity (eg corticosteroid tx, malignancy), decr cough reflex post op, decr mucociliary clearance
b. aspiration of nasopharyngeal or gastric secretions – immobility, decr consciousness, vomiting
c. introduced bact – eg ETT
d. bacteraemia – eg abdo sepsis
4. Organisms – Escherichia, pseudomonas, klebsiella, S.aurues, anaerobes
5. Presentation (similar to CAP) - Cough, sputum purulence, fever, dyspnea, central cyanosis, crackles
6. Ixs – CXR mottled opacities in both lungs
7. Mgt – A/B G- cover – 3rd gen cef (cefotaxime) + Gent / Physio
8. Prog – 30%

Aspiration Pneumonia
1. Def – a bronchopneumonia developing from foreign material in bronchial tree, usu oral/gastric contents (incl food, saliva, nasal secretions)
2. Pathophysiology – either chemical pneumonitis or bacterial (anaerobic) infection/inflammation
3. Aspiration risks – GA, excess ETOH, head injury, CVA, seizures, coma
Complication of Aspiration = Lung Abscess (pus formation in newly formed capsule)
1. Def – Localised area of lung parenchymal necrosis where inf by a pyogenic organism casues tissue necrosis + suppuration
2. Etiology – aspiration (alcohol most common cause), epileptics, bronchial obstruction (eg ca)
3. Organisms – mixed, predominantly anaerobes
4. Presentation
a. Hx of aspiration
b. Systemic – fever, sweats, lassitude, anorexia, weight loss
c. Productive cough
d. Dyspnea
e. CP
f. Hemoptysis
5. Ix
a. CXR parenchymal infiltrate, 1+ areas of homogenous density with air-fluid levels
b. CT gold standard
6. Mgt
a. As per aspiration pneumonia; Co-amoxy 1.2 Q8H + Metronidazole 500 mg Q8H
b. Surgical draining may be reqd

Empyema (pyothorax) (pus formation in natural body cavity)
1. Def – presence of pus in the pleural cavity
2. Etiology – arises from pneumonia associated with a parapnemonic effusion
3. Organisms – mixed anaerobes
4. Stages
a. Exudative – accumulation of pus
b. Fibrinopurulent – loculation of pleural fluid
c. Organising – scarring, potential for lung entrapment by scarring → pulmonary fibrosis + cor pulmonale
5. Presentation
a. Fever
b. CP
c. Cough
d. Dyspnea
6. Physical examination – a. clubbing, b. percussion dullness, c. decr breath sounds
7. Ixs
a. CXR – pleural effusion
b. US – confirms size/location of abscess + presence of fibrin aggregates
c. Thoracentesis – confirmation of dx (ph <7.2, Glucose <2.2, +ve G stain or culture)
8. Mgt
a. Avoid delays – prevent progression to organising phase
b. ICT – drain pus from pl space
c. A/Bs – co-amoxy + Metro as per lung abscess 4-6 weeks
d. Surgical debridement – if med tx fails

Pleural Disease

Pleural Effusion
1. Definition
a. Excessive accumulation of fluid in pl space
b. Clinical detection >500 ml
2. Etiology
a. Transudates (hydrostatic forces, no ∆ pleural membrane)
i. LV failure
ii. Cirrhosis / Hypoalbuminaemia
iii. Constrictive peritonitis
iv. Nephrotic syndrome
b. Exudates (inflammation and capillary leak or impaired lymphatic drainage, ↑ pl membr perm)
i. Bacterial pneumonia
ii. Carcinoma of the bronchus (massive effusions typically malignant in origin)
iii. TB
iv. Trauma
3. Presentation
a. Sxs
i. Asx (if small)
ii. Pleuritic CP
iii. Dyspnea
iv. Cough
b. Signs
i. ↓ chest wall mvment
ii. ↓ VR / fremitus (cf ↑ in consolidation)
iii. percussion stony dull
iv. absent breath sounds
4. Ixs
a. CXR – blunting of costophrenic angle
b. Pleural fluid aspiration – unless clinical picture clearly suggests a transudate (eg HF pt w bilateral pl effusion)
i. Diagnostic and Sx relief
ii. Microbial analysis – G stain + culture
iii. Cytological analysis – differential wcc, malignant cells
c. Contrast enhanced CT – if fluid aspirate non-diagnostic
i. Identification of pleural nodularity/thickening (malignancy)
ii. Image guided needle biopsy of focal areas of abnormality
d. Pleural biopsy
i. Blind percutaneous biopsy performed if Ø abnormalities on CT → tissue sent for TB smear, culture, histology
5. Management
a. Transudates → tx underlying cause
b. Exudates → drainage
c. Malignant effusions usu re-accumulate after drainage → drain until dry, add sclerosing agent into space

Pneumonthorax
1. Definition
a. PTX - Air in pleural space
b. Tension PTX – pleural tear acts as a 1 way valve, air only passes on inspiration, pos pressure buildup lead to cardiorespiratory impairment and eventual cardiac arrest
2. Etiology
a. Spontaneous primary PTX
i. Ø underlying lung dis
ii. Typically healthy tall males 25-35 at rest or during normal activites – usu smokers and familial tendency
iii. Most common cause thought to be rupture of subpleural bleb (acqd lung cyst, usu <1 cm diam, smaller than a bulla)
b. Secondary PTX
i. Assoc w underlying lung dis – COPD, trauma
3. Pathophysiology
a. Loss of negative intrapleural pressure → ↓ VC → PaO2 → low V/Q
4. Presentation
a. Sxs
i. Sudden onset pleuritic CP (stabbing)
ii. Dyspnea
b. Signs
i. ↓ chest expansion
ii. ↓hyper-resonance
iii. ↓ breath sounds
c. Signs of a tension ptx
i. Distress
ii. Tachycardia
iii. Tachypnea (due to combined hypoxia and ↓ CO)
iv. Mediastinal / Tracheal shift to opposite side
5. Ixs
a. CXR
i. 2cm from lat edge of lung to inner wall ribs → 50% of lung
ii. >2 cm = large / <2 cm = small
iii. ?mediastinal shift
b. CT – to differentiate severe bullous lung dis from ptx and prevent potentially dangerous needle aspir in bullous emphysema
6. Management by sxs
a. Observation + O2 – if Ø underlying lung dis, small (<2cm) ptx, Ø dyspnea, appropriate social circumstances – 1.25% resol/day, to return if breathless
b. Aspiration – Ø if secondary ptx (ie underlying lung dis)
c. ICT (intercostal tube) insertion – if underlying lung dis
7. Management by etiology
a. Spontaneous primary ptx
i. High flow O2 – 10 l/min
ii. Ø breathlessness or <2cm on cxr → d/c + return on breathlessness
iii. Or 2x attempts at aspiration + d/c
iv. If unsuccessful – ICT
v. Ø smoking
b. 2ndry ptx
i. admission
ii. single aspiration attempt only if minimally breathless + <50 yrs + small ptx
iii. chest drain insertion in all other pts

Venous Thromboembolism (VTE) and Pulmonary Embolus

Thromboembolism risk factors
1. Virchows Triad
a. Alterations to blood flow – stasis (travel, immobilisation, pregnancy)
b. Injury to vascular endothelium
c. Alterations in the constitution of blood - hypercoaguability
2. Trauma
3. Age
4. Malignancy

DVT
1. Presentation
a. Swollen, warm tender calf or thigh
b. Hx of RFs – eg overseas travel or recent surgery/injury
c. Homan’s sign +ve – pain in calf when ankle slowly dorsiflexed (w knee bent)
2. Differentials
a. Cellulitis
b. Ruptured bakers cyst
c. Edema from other causes
3. Ixs
a. D-dimer (product of fibrin degradation)
i. High negative predictive value (but many false positives) – used for screening but not diagnosing
b. Doppler US – reduced venous flow in deep venous sys (confirmation of dx), not reliable for calf vein thrombosis
c. Venography – reqd for calf vein thrombosis
4. Tx
a. Below knee – compression bandage (v low risk of embolus), ?6/52 anticoag may be recommended
b. Above knee – anticoagulation for 3/12 (unless specific RF eg bed rest, then only 4/52 reqd)
c. Anticoagulation – initially heparin, then warfarin
5. Complications of DVT
a. PE
b. Post thrombotic syndrome – permanent pain, swelling, edema resulting from destruction of the deep valves (elastic support stockings helpful)
c. Recurrence of thrombosis

PE
1. Definition – embolism of pulmonary arteries, commonly a complication of DVT (occurs in ~30% of DVT pts)
2. Pathophysiology
a. Large embolus → obstruction of pulmonary artery → distal pulmonary infarction
b. Causes hemodynamic changes → pulm HTN, ↑ RV filling pres + corpulmonale
c. Hypoxaemia due to V/Q mismatch – vent but no perfusion
d. Death in ~10%
3. Presentation
a. Small / Medium PE
i. Dyspnea
ii. Pleuritic CP
iii. Hemoptysis (if there is pulmonary infarction)
iv. O/E – tachypnoeic, pleural rub, exudative blood stained pleural effusion may develop
b. Massive PE
i. Severe central CP
ii. Sudden shock, pale, sweaty
iii. Marked tachypnea and tachycardia
iv. Syncope + death
v. O/E – central cyanosis, JVP elev, hypotension, RV heave, accentuation of S2
4. Ixs → Radiological evidence is necessary for a PE dx
a. ABG – hypoxaemia, hypocapnia
b. ECG and CXR – helpful to exclude differentials
c. D-Dimer – negative d-dimer only excludes those pts w a low clinical probability
d. V/Q scan – helpful if either normal or strongly positive (usu not), unsuitable for pts w pre-existing lung dis
e. US – detection of clots in pelvic or iliofemoral veins
f. CT pulmonary angiography (CTPA) (gold standard) - Equiv results but greater access and patient comfort cf to pulmonary angiography
5. Patient approach
a. Clinical suspicion of PE → D-dimer (if negative, stop and consider other dxs)
b. If positive and tx planned → CTPA (stabilise a hypotensive or hypoxaemic pt prior to CT) - stop tx if negative
6. Management (tx started on clinical suspicion pending ix)
a. O2 if hypoxaemic
b. IVF +/- ionotropes – to raise filling pres
c. Dissolution of thrombus (Streptokinase) → for massive embolism with hypotension + signs of acute R heart strain (can be given with heparin)
d. Analgesia – Morphine to relieve pain + anx
e. Prevention of further emboli - LMWH + Warfarin (IV heparin bolus initially followed with oral warfarin 5-10mg daily – aim for IN 2.5, continue 3-6/12)
f. IVC filter – recurrent PE while anticoagulated
g. LT management – RF mgt, repeat imaging at 6-12 wks

Diffuse Parenchymal Lung Disease (DPLD) – aka Interstitial Lung Disease (ILD)

1. Definition
a. A wide variety of diseases affecting the parenchyma fo the lung
b. Classified together bec of their similar clinical, radiographic, physiological or pathogenic manifestations
2. Aetiologies
a. Idiopathic – eg pulmonary fibrosis
b. Environmental – eg asbestosis (lag time 20 yrs)
c. Drug – eg amiadorone, methotrexate
d. Systemic disease – interstitial pn as part of a CT dis such as rheumatoid, SLE, scleroderma
e. Other – eg sarcoidosis
3. Presentation
a. Sxs
i. Older (except sarcoidosis)
ii. Asx w abnormal cxr
iii. Insidious onset dyspnea and dry cough
iv. Ø wheeze
v. Failed tx for infection + HF common (main differentials)
b. Signs
i. ↑ RR
ii. Cyanosis or ↓ O2 sat
iii. Clubbing
iv. ↓ chest expansion
v. Fine Velcro-like crackles (esp lung base)
4. Ixs
a. Spirometry – restrictive lung volumes
b. CXR
c. HRCT (high res CT)
5. ILD physiology
a. Small stiff lungs
b. Restrictive lung vol - ↓TLC, ↓ VC, Preserved FEV1/VC ratio, Normal airflow at all lung volumes
c. ↓ Diffusion, ↓ lung compliance, widened Aa gradient
6. IPF (idiopathic pulmonary fibrosis) – archetypal ILD
a. Def - Progressive pulmonary fibrosis – median survival <3 yrs
b. Epidem - Older pts – typically blue collar workers
c. Etiology – unknown
d. Dx via HRCT
e. Current txs - ineffective
f. Case – 57M, PC 2 yr hx of ↑ breathlessness + dry cough, worked as metal polisher, o/e- clubbed + fine crackles
7. Sarcoidosis
a. Def – multisystem granulomatous disease commonly affecting mediastional/hilar nodes and lung parenchyma
b. Etiology – unknown
c. Epidem – typically younger, Ø children
d. Tx – steroids effective, no cure
e. Rarely fatal but can cause sig and permenant disability
f. Lofgrens syndrome – erthema nodosum, arthralgias, hilar L/A
g. Case – 26F, PC-acute onset fatigue, painful rash on legs, aching/swelling of ankles and knees + abnormal cxr → presents two years later w exertional SOB + dry cough

Lung Cancer

1. Epidemiology
a. Most common of cancer death in men
b. ↑ in women
2. Etiology
a. Smoking – 10x ↑ risk, dose-response r/ship
b. Asbestos
3. Classification
a. Non-small cell lung carcinoma
i. Squamous cell carcinoma
1. Epidem - 30% of lung ca
2. Pt - >45 yrs age, smokers
3. Pres – obstructive lesions, mets occur late (slow growing)
4. Assoc w cavitation and hypercalcemia
ii. Adenocarcinoma
1. Epidem - 15-40% of lung ca, ↑ incidence
2. Pt – proportionally more common in non-smokers (20%)
3. Pres – more variable
iii. Large cell (undifferentiated) carcinoma
1. 15% of lung ca
2. Early mets
3. Poor prognosis
b. Small cell carcinoma
i. 10-20% of lung
ii. Propensity for early mets
iii. Arise from endocrine cells → propensity to secrete hormones (paraneoplastic syndrome)
1. ACTH → Cushings
2. PTH → Hypercalcemia
3. ADH → SIADH
4. Presentation
a. Local endobronchial spread and peripheral growth
i. Cough
ii. CP
iii. Hemoptysis
iv. Dyspnea
v. Wheeze / Stridor
b. Regional spread
i. Brachial plexus → shoulder / inner arm pain
ii. Sympathetic ganglion → horners
iii. Recurrent laryngeal nerve → hoarseness, bovine cough
iv. SVC obstruction
v. Dysphagia
c. Metastatic
i. Lethargy, Malaise
ii. Weight loss
iii. Appetite loss
d. Paraneoplastic syndromes
5. Ixs
a. Confirm dx
i. CXR – 95% will be abnormal
1. Round shadow with fluffy or spiked edges
2. Cavitation, lobar collapse, pl effusion, 2ndry pneumonia
b. Determine histology
i. Sputum cytology – malignant cells, require 3x specimens, 60-80% positive in central tumors, less for peripheral tumours
ii. Bronchoscopy – obtain biopsies for histology
iii. Transthoracic FNA biopsy (radiographic guided) – tissue dx from peripheral tissues
c. Assess spread of tumour → bronchoscopy, CT
6. Management
a. NSCLC
i. Surgery – only 10% of pts operable, stage 1-2 potentially curable
ii. Radiotherapy – curative intent for stage 1-2 whom unfit for surgery, all others palliative
iii. Chemotherapy – palliation for unresectable stage 3-4, combination chemo, ↑ survival for a few months but improved QOL and sx control
iv. Prognosis – 5 yr survival
1. Stage 1 - 60%
2. Stage 2 – 40%
3. stage 3 – 10%
4. Stage 4 - <2%
b. SCLC
i. 70% present with mets → surgery Ø an option
ii. Chemo + Radiotherapy – palliative intent
iii. Considerable improved life expectancy with tx vs no tx

Asthma

1. Definition – a chr inflammatory condition of the lung airways characterised by –
a. Airflow limitation
b. Airway hyper-responsiveness
c. Airway inflammation
2. Epidemiology – 10-15% affected in 2nd decade of life
3. Etiology
a. Atopy – those who readily develop IgE antibodies to common etal antigens (dust mite, grass pollen)
b. ↑ responsivness of airways – as measured by ↓ FEV1 to stimuli such as inhaled histamine (bronchial provocation test)
4. Pathogenesis
a. Primary abnormality → airway narrowing
i. SM contraction
ii. Thickening of a/w wall (hypertrophy, edema)
iii. Secretions (mucus hypersecretion)
b. Remodelling
i. SM hypertrophy
ii. Epithelial metaplasia with ↑ numbers goblet cells
5. Precipitating Factors
a. Allergen – dust mite fecal particles
b. Viral infection
c. Cold air
d. Exercise
e. Irritant dusts, vapours etc
f. Emotion
g. Drugs – NSAIDs, aspirin, b-blockers
6. Clinical features
a. Sxs (typically worse at night)
i. Wheeze (non-specific to asthma)
ii. Coughing
iii. Chest tightness
iv. SOB
b. Signs during an attack
i. ↓ chest expansion
ii. prolonged expiratory time
iii. bilateral expiratory wheeze
7. Differentials
a. COPD – Ø reversible, 50+ age, smoking hx, steroid trial ineffective
b. Bronhiectasis
c. Brochiolitis
d. Large a/w obstruction – eg endobronchail tumor, foreign body
e. Hyperventilation syndrome
f. DILD
8. Asthma Control
a. Assessing asthma control → a. blue inhaler use, b. night waking, c. exercise tolerance
b. Reasons for poor asthma control → a. non-complaince with steroids, b. incorrect inhaler use, c. domestic/occupational factors
9. Ixs
a. Demonstration of variable airflow limitation
i. Spirometry - FEV1 – 15%∆ and >200 ml
ii. PEFR - ↑ after bronchodilator (20% improvement or >60 L/min from baseline)
b. Histamine (or methoacholine / hyertonic saline) challenge - ↓ FEV1 demontrated
c. Measure exhaled nitric oxide – iNOS related
d. Skin prick tests – allergen identification after injection into epidermis of forearm
e. CXR – only at dx or in severe attack
f. Steroid trial – Prednisone 30 mg daily for 2 wks (given to all pts w severe airflow limitation), improvement in FEV1 >15% confirms reversibility and indicates potential benefit of inhaled steroids
10. Managemenet
a. Education + Flu vaccine
b. Avoidance of precipitating factors – Ø smoking, pets, household cleaning, occupational, b-blockers
c. Drug Tx (in stepwise order)
i. SABA (B2 agonist) → relax bronchial smooth mus → brochodilation
1. Salbutamol (ventolin) PRN
a. Onset 5 mins, Action 4-6 hrs
b. Side effects – tremor, tachycardia (↓ as tol develops, a/ws less affected by down-reg due to ↑ R density)
2. Terbutaline
ii. Antimuscarinic bronchodilators → ipratropium bromide (additive to SABA)
iii. Inhaled steroids (added if symptomatic >1x /day) – maintenance in all but mild cases
1. Beclomethasone (Beconase) – 200 ug bd
2. Budesonide – 200 ug bd
3. Fluticasone 50/125 ug bd
4. Regular use reqd – days/weeks reqd to reach full effect
5. Side effects – oral candidiasis, hoarseness
iv. LABA (add on only)
1. Salmeterol (serevent)
2. Eformeterol (oxis)
3. bd dosing – can ↑ dose up to 2000 ug/day
4. duration action 12 hrs
v. Combinations
1. symbicort = budesonide + eformeterol
2. seretide = fluticasone + salmeterol
vi. If ineffective and steroid dose at max 2000 ug/day
1. LTRA (leukotriene R antagonist)
2. Theophylline
3. Oral steroids (prednisone)
11. Acute severe asthma
a. Approach to acute moderate asthma (PEFR 50-75% of predicted)
i. Nebulised b-agonist
ii. D/c after 1 hr of stability w a tapering dose of prednisone (starting at 40 mg daily)
b. Clinical features of severe asthma
i. Inability to complete one sentence with one breath
ii. RR >25 /min
iii. Tachycardia >110 bpm
iv. PEFR 33-50% of predicted
c. Life threatening features
i. Silent chest
ii. Cyanosis
iii. Exhaustion
iv. Confusion / Coma
v. Bradycardia
vi. Hypotenson
vii. PEFR <30% predicted (~150 L/min in adults)
viii. ABG – PaO2 <8 kPa, O2 sat <92% despite O2 tx

COPD

1. Definition (2 parts)
a. Grp of diseases characterised by airflow limitation of airway that is not fully reversible
b. Airflow limitation is progressive and assoc w an inflammatory response of the lungs to noxious gases
2. Epidem
a. 5% adult popn
b. 4th most common COD
3. Etiology and Pathophysiology
a. Smoking → activation of mphages → neutrophil chemotactic factors
b. Neutrophils + mphages → release proteases → b/down of lung parenchyma → emphysema + mucous hypersecretion
c. Proteases normally countered by protease inhibitors (eg a1-antitrypsin) → tipped in favour of proteolysis
4. Clinical features
a. Sxs
i. Cough
ii. Sputum production
iii. Wheeze
iv. Dyspnea
v. Frequent infective exacerbations
b. Signs
i. Breathless at rest
ii. Hyper-inflated lungs
iii. Prolonged expiration
iv. Use of accessory breathing muscles
v. Poor chest expansion
vi. Pink puffers – predominant sx = breathlessness
vii. Blue bloaters – hypoventilation, cyanosis, edema
5. Dx – no single diagnostic test, dx via hx, exmn and confirmation of airflow limitation with lung function testing
6. Ix
a. CXR
b. Bloods - ↑ Hb, ↑ PCV (persistent hypoxaemia with 2ndry polycythemia)
c. ABG
d. Lung function tests
i. ↓ FEV1 - <80% of predicted
ii. ↓ FEV1/FVC Ratio - <0.7
iii.
e. ECG / Echo – if features of cor pulmonale
7. Differentials
a. Asthma
b. Lung ca
c. Bronchiectasis
d. HD
e. ILD

Chronic Bronchitis (blue bloater)
1. Definition – Clinical Diagnosis
a. Cough + excessive mucus prodn
b. >3 months in at least 2x consecutive years
c. Ø due to any other dis/condition
2. Pathology
a. Mucus gland enlargement → hypersecretion → obstruction
b. Irritation → inflammation + edema → scarring + remodelling → wall thickening → airway narrowing
c. Superadded infection
3. Presentation
a. Sxs
i. Dyspnea
ii. Productive cough
iii. Frequent respiratory infections that worsen the sxs
b. Signs
i. Cyanosis - ↓ Hb sat
ii. Edema / Congestion – due to pulmonary HTN resulting in cor pulmonale
iii. Asterixis – CO2 retention
iv. Plethoric face – 2ndry polycythemia
v. Wheeze
vi. Crackles
4. Ixs
a. Pulse ox
b. ABG → ↓ PaO2, ↑ PaO2 (may have lost hypercapnic drive and be relying on hypoxic drive)
c. FBC
d. CXR
e. Spirometry → ↓ FEV1, ↓↓ FEV1/FVC Ratio
5. Complications
a. Cor pulmonale - early
b. Pneumonia
c. Respiratory failure
d. Cardiac arrhythmias

Emphysema (pink puffer)
1. Definition – “histological diagnosis” - Enlarged air spaces distal to terminal bronchioles with destruction of alveolar wall
2. Pathology
a. ↑ elastase activity → alveolar wall destruction → enlargement of air spaces → ↓ recoil
b. ↓ surface area → ↓ O2 transfer → dyspnea
c. Small airways collapse during expiration → airflow obstruction
d. Hypercapnic drive → hyperventilation allows maintenance of almost normal ABGs
3. Presentation
a. Thin - ↑ rate of work
b. Anxious
c. Tachpnea
d. ↓ I/E ratio
e. Pursed lip breathing
f. Accessory breathing muscle use, intercostal indrawing
g. Hyperinflated chest
h. ↓ chest expansion
i. Hyper-resonance
4. Ixs
a. ABGs → often normal, may have ↓ PaO2, ↓ PaCO2
b. Spirometry → ↑ TLC, ↓ FEV1
5. Complications → late cor pulmonale

Management of COPD - COPDX
1. Confirm dx and assess disease severity
2. Optimise function
a. Inhaled bronchodilators – SABA, Ipratropium
b. LABA – moderate to severe COPD
c. Inhaled glucocorticoids (fluticasone) for severe COPD w freq exacerbations – Oral not recommended LT
d. Pulmonary rehab
e. Diuretics if cor pulmonale
3. Prevent deterioration
a. Ø smoking
b. Flu / Pneumococcus vaccine
c. LT O2 therapy – 15 hrs per day in hypoxaemic pts PaO2 <7.3 kPa
4. Develop support network and self mgt plan – breathe deeply and slowly
5. Manage exacerbations
a. A/Bs – cefaclor, co-amoxyclav (hx of purulent sputum or cxr ∆s)
b. Systemic glucocorticoids in acute exacerbations only – prednisone 30 mg po 2 wks
c. Non-invasive pos pres vent in hypercapnic vent failure
d. Fixed O2 delivery – 28% at 2 L/min for hypoxaemia

Respiratory Failure
1. Type 1 - ↓ O2 <6 kPa
a. Dyspnea
b. Central cyanosis
c. Restlessness, Agitation
d. Confusion
2. Type 2 - ↑↑ CO2
a. Headache
b. Peripheral vasodilation
c. Tachycardia
d. Asterixis
e. Confusion
f. Drowsiness and coma

Cor Pulmonale
1. Def – RH failure due to pulm HTN
2. Etiology – COPD most common cause, others incl pulm vascular d/os
3. Presentation - ↑ JVP, pulsatile liver, edema
4. Ixs
a. ↑ Hb, ↑ Haemotocrit
b. ABG – hypoxaemia w or w/o hypercapnia
c. CXR – enlarged RA/RV, prominent pulm arteries
d. ECG – r axis deviation, RVH

Sleep Disorders and Sleep Disordered Breathing

1. Insomnia – perception that sleep is inadequate, usu in quantity
a. Acute - <3 wks duration (very common in types of stress, usu self limiting)
b. Chr - >3 wks
i. Primary – type A personality, mental illness hx, thoughts/anxiety re sleep
ii. 2ndry
1. Physical illness – eg pain syndrome
2. Mental illness – eg depr
2. Snoring and OSA
a. Apnoeas – pauses in breathing, usu brief, prolonged apnoeas (>10s) are potentially pathological
b. Hypopneas – shallow breathing, ?significance
c. Snoring – indicates upper a/w narrowing sufficient to cause turbulence with resultant vibration of upper a/w walls and soft palate
d. OSA
i. Definition
1. Apnoeas due to upper a/w narrowing or full obstr leading to clinical sxs
2. Episodes disrupt sleep leading to excessive daytime sleepiness (EDS)
ii. Epidem – 2-4% of middle aged men, 1-2% of females some degree of OSA, ↑ risk in M/PI
iii. RFs
1. Shape of throat – eg retrognathia
2. BMI – fat neck, obesity
3. Age - ↑ collapsibility of throat with age
4. Male
iv. Presentation
1. Sleepiness
2. Difficulties with conc and memory
3. Dry mouth on wakening (blocking off of saliva)
v. Tx
1. Weight loss
2. Positional – keep subject off back may be helpful
3. CPAP – only reliable proven tx for OSA, splints a/w preventing narrowing
4. Surgery – limited success, rarely used on pts w a normal face shape
5. Mandibular advancement devices – occasionally successful for mild OSA or snoring only
vi. Complications of OSA → HTN → LT CVS damage with ↑ risk of strokes / MI

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