Asthma = recurrent episodes of dyspnoea, cough and wheeze - Precipitants, differential dx and exam findings
Precipitants
o Cold, exercise, emotion, allergens, infection, smoke, NSAIDS, B blockers
Exam findings
General - Tachypnoea, Audible wheeze
Peripheries and Face (nasal polyps?)
Chest
- hyperinflated chest
- hyper-resonant percussion
- diminished air entry
- longer expiration
- widespread polyphonic wheeze
DIFFERENTIAL DIAGNOSIS
- COPD
- Large airway obstruction or SVC obstruction
- Pneumothorax or PE
- Bronchiectasis or obliterative bronchiolitis
- Sinusitis
- Foreign body aspiration
IX and management of asthma (acute + chronic )
INVESTIGATIONS
Acute Attack
- Bloods: FBC, U+E, CRP, cultures, ABG
- Peak flow, Sputum culture, CXR
Chronic
- Peak expiratory flow monitoring - Diurnal variation
- Spirometry
o Obstructive defect (low FEV1/FVC, low residual volume)
o > 15% increase in FEV1 following B agonist. - CXR ->Hyperinflation
- RAST testing (radioallergosorbent test to detect specific IgE abs to determine allergy
- Aspergillus serology (IgE)
MANAGEMENT
Acute:
-Nebulized salbutamol
-Oxygen
-Hydrocortisone or prednisolone
-If persisting – add ipratropium nebs and give
magnesium sulphate
Chronic
Non-Pharmacological
- Smoking cessation
- Avoidance of precipitants
- Twice daily PEF
- Written emergency action plan
SMART therapy:
o Budesonide (ICS)/formoterol (LABA)
o used for maintenance
and relief of sx prn
Can add on for poor control with SMART:
1. Leukotrine receptor antagonist (Oral Monteleukast) or theophylline
2. Oral prednisone
3. Tiotropiumbromide (LAMA)
Bronchiectasis - causes, exam, complications, differentials
CAUSES
Primary (congenital)
- Cystic fibrosis
- Primary cilia dyskinesia
- Congenital hypogammaglobulinemia
Secondary (acquired)
- childhood infection (TB, pneumonia, measles, whooping cough)
- Localized disease (bronchial adenoma, TB, foreign body)
- Allergic bronchopulmonary aspergillosis
- Rheumatoid arthritis
- COPD
- Recurrent aspiration
- ILD and pneumoconiosis
- Idiopathic 50%
EXAMINATION
General Observation
- Unpleasant sputum
Hands ttyy- Clubbing
Chest
- Position of apex beat
- Wheeze
- Crackles insp, gurgly noises
- RHF sx
- Pectus carinatum
Associated conditions to looks for: rheumatoid
arthritis, IBD, CF,GORD
Consider the following complications and look for
them:
- Pneumonia
- Pleurisy
- Empyema
- Lung abscess
- Cor pulmonale
- Amyloidosis
DIFFERENTIAL DIAGNOSIS
- Chronic bronchitis
- COPD
- TB
- Asthma
IX and management of bronchiectasis
INVESTIGATIONS
- Chest X-Ray
o Cystic lesions
o Streaky infiltration
o Thickened bronchial walls
- Sputum microscopy and culture
o Common organisms are
haemophilus influenzae,
pseudomonas, Escherichia coli, pneumococcus, mycobacteria, staph
aureus - Testing for cystic fibrosis (sweat test) and
immotile cilia syndrome in young adults - Spirometry
o For assessing severity not diagnosis
o FEV1 < 40% severe - High resolution CT
o Confirms diagnosis
o Perform when patient stable
o Airway dilatation diameter greater
than accompanying pulmonary artery) - Bronchoscopy (to locate site of haemoptysis
and obtain sample for culture) - FBC and IgE for Aspergillus
MANAGEMENT
-Twice daily postural drainage
- Physiotherapy
- Influenza and pneumococcal vaccines
- Smoking cessation
- Home oxygen may be offered to nonsmoking patients with severe disease (FEV1 < 40%) and oxygen saturation <93% on RA.
Pharmacological
- Antibiotics
o During exacerbations, use according to sensitivities, if >3/year consider long term abx
- Bronchodilators: Facilitate clearance of sputum
- Treatment of heart failure
Invasive
- Surgery if localized disease or severe haemoptysis
- Transplant is occasionally appropriate for end stage disease
COPD exam and investigations
General Observation
- Pursed lip breathing, use of accessory muscles
- Prolonged forced expiratory time
- Sputum pot
- Signs of cachexia
- Tachypnea
Hands
- Cyanosis, polycythemia
- Asterixis if CO2 retention
Face and Neck
- Cyanosis
- Tracheal tug
- Reduced cricosternal distance (<3cm)
Chest
- Inspection: Intercostal recession, Increased AP diameter-barrel chest
- Palpation/Percussion
Reduced chest wall
movement/chest expansion
, Hyper-resonant percussion - Auscultation
o Reduced breath sounds
o +/- wheeze
o Early course inspiratory crackles
INVESTIGATIONS
Spirometry is required to make a diagnosis in this
clinical context (obstructive)
- Post bronchodilator FEV1/FVC < 0.7 confirms persistent airflow limitation
- (mild) – FEV1 > 80% predicted
- (moderate) – 50% FEV1 <80%
-(severe) – 30% FEV1 < 50%
- (very severe) – FEV1 < 30%
- CXR – hyperinflation (>6 anterior ribs seen, flat hemidiaphragms)
- ECG – RVH from cor pulmonale
- ABG – PaO2 decreased, with or without hypercapnia
- FBC – exclude secondary polycythemia
Assessment of COPD (3 aspects in hx and exam)
Symptoms
- Degree of airflow obstruction (using
spirometry)
- Risk of exacerbations
o Precious exacerbations, how many per year, hospital admissions, ICU admissions. - Treatment
o Use of prednisone, how long inhalers last for. - Comorbidities
o CVD, osteoporosis, depression and anxiety, skeletal muscle dysfunction,
metabolic syndrome, lung cancer.
Differential dx for dyspnoea for lung diseases onset, hx, sx worse
- COPD
o Onset mid life
o Symptoms slowly progressive
o History of tobacco smoking or exposure - Asthma
o Onset early in life
o Symptoms vary widely from day to day
o Symptoms worse at night/early morning
o Allergy, rhinitis and/or eczema also present
o Family history of asthma - Congestive Heart Failure
o Fluid overload
o CXR shows A – alveolar oedema (bats wings), B – kerley B lines (interstitial oedema), C – cardiomegaly, D – dilated, prominent
upper lobe vessels, E – pleural effusion.
o Pulmonary function tests indicate volume restriction not airflow limitation - Bronchiectasis
o Large volumes of purulent sputum
o Commonly associated with bacterial infection
o Chest X-ray/CT shows bronchial dilation, bronchial wall thickening - Chronic Bronchitis
o Cough and sputum production for at
least three months in each of two consecutive years, not necessarily associated with airflow limitation - Tuberculosis
o Onset all ages
o CXR shows lung infiltrate
o Microbiological confirmation
o High local prevalence
Aim of COPD treatment
C – Confirm the diagnosis
- O – Optimize function
- P – Prevent deterioration
- D – Develop a plan of care
- X – Manage exacerbations
Chronic treatment of COPD - pharm for less symptoms, more symptoms
Non-Pharmacological
- Smoking cessation
- Pulmonary Rehab
- Physical Activity
- housing and nutrition
- Flu Vaccine/ pertussis/pneumococcal
Pharmacological
Less symptoms, low exacerbation risk
LAMA. (eg. incruse ellipta umeclidium)
- If needed move to LABA/LAMA
Spiolto respimat - tiotroprium olodaterol
HIgh exac risk start with same but can move to
- ICS/ LABA if eosinophilia eg. seretide, breo
- LABA/LAMA/ICS eg. trelegy ellipta
Asthma COPD overlap
- ICS LABA pluse LAMA
- (Long term monotherapy with oral and inhaled corticosteroids is not recommended. Increased risk of pneumonia)
- If cor pulmonale = diuretics
Ix and treatment of acute exacerbation of COPD
Investigations
- ABG
o Pa02 < 8.0kpa =Resp Failure
o PaC02 <6.7kpa =Type I Resp Failure
o PaC02 > 6.7kpa = Type II Resp Failure
(CO2 only increases when
global ventilation affected)
- CXR
o Exclude other diagnoses - ECG
o Aid in diagnosis of coexisting cardiac problems - Bloods
o FBC – polycythemia or bleeding
o U+E – electrolyte disturbance, diabetes, poor nutrition - Spirometry not recommended
Treatment
- Oxygen
- Short acting inhaled beta agonists +/-short
acting anticholinergics (i.e. salbutamol nebs + ipratropium nebs)
- Systemic corticosteroids
- Antibiotics should be given to patients (if evidence of infection)
o Febrile with elevated WCC and consolidation on CXR
o Amoxicillin
o Sputum culture not required unless not responding to tx - Aminophylline if not responding
- Adjunct therapies
o Fluid balance
o Physiotherapy to clear sputum
o Attention to medication particularly diuretics and anticoagulants
o Treatment of comorbidities
o Smoking cessation advice
Consideration of DVT and PE risk, thromboprophylaxis measures.
Interstitial lung disease causes and exam
Known cause
- Occupational
o Asbestosis
o Silicosis
o Bird poo
o Coal
radiotherapy , fungal spores
- Drugs
o Methotrexate, amiodarone - Hypersensitivity
o Extrinsic allergic alveolitis -> granuloma - Infections
o TB granuloma
o Fungal
Associated with systemic disorders
- Sarcoidosis granuloma
- Rheumatoid arthritis
- Connective tissue diseases e.g. SLE, Sjogren’s syndrome, systemic sclerosis
- Ulcerative colitis, renal tubular acidosis,
autoimmune thyroid disease
Idiopathic
- Idiopathic pulmonary fibrosis (most common cause of ILD)
- Cryptogenic organizing pneumonia
- Lymphocytic interstitial pneumonia
EXAM
General
Peripheries and Face
- Clubbing
- Cyanosis
Chest
- Velcro fine crackles, ↓02, ↑RR
- Signs of pulmonary hypertension
o Elevated JVP with large V wave
o Parasternal impulse (RV heave)
o Tricuspid regurgitation
Other
- Signs of systemic disease
Ix and treatment of Interstitial lung disease
INVESTIGATIONS
- Imaging
o CXR - may be normal, decreased lung volume, diffuse opacity
o High Resolution CT
Localised or Diffuse e.g. honeycomb lung of IPF (sometimes seen on
CXR)
Essential for diagnosis
Pleural thickening e.g.
asbestosis
- Spirometry
o Usually reveal restrictive patterns (low FEV1, v low FVC, normal/high FEV1/FVC) - Bloods
o FBC – high ESR/CRP, eosinophilia
o Hypogammaglobulinemia
o Raised LDH
o Rheum serology – ANA, RF
o ABG – low Pa02 normal or high PaCO2. Wide Aa gradient
- Bronchoalveolar lavage
o Increased lymphocytes –> active inflammation thus more likely to respond to treatment and better prognosis e.g. drug induced, EAA, acute granulomatous disease
o Polymorphonuclear cells (basophils, eosinophils, neutrophils) – more likely to not respond to treatment, poorer prognosis - Biopsy
o Transbronchial
Rule out infection
Sarcoidosis
Lymphangitic spread of
carcinoma
o Thorascopic
For diagnosis of idiopathic
ILD if clinical uncertainty
and result could change management.
TREATMENT
Non-Pharmacological
- smoking cessation
- remove exposure
- pneumococcal and influenza vaccine
- home 02 for symptomatic relief of hypoxic patients
- pulmonary rehab
Pharmacological
- Treatment will not reverse established fibrosis
- If active inflammation, treatment may help.
Steroid (1mg/kg/day, reduced to half after 4-12 weeks) with follow up spirometry to document response. Consider maintenance steroids for patients who improved or stablised. NOT for idiopathic
- Immunosuppressive agents for sarcoidosis, mesothelioma, secondary to inflammatory/rheumatoid condition
- Unilateral lung transplantation considered in final stages esp. IPF.
- Palliative care input
Lung cancer complications (local, metastatic) and exam
COMPLICATIONS
Local
- Recurrent laryngeal nerve palsy
- Phrenic nerve palsy
- SVC obstruction
- Horner’s Syndrome (Pancoast’s tumour)
- Rib erosion
- Pericarditis
- AF
Metastatic
- Brain
- Bone - >anaemia, high Ca
- Liver
- Adrenals -> Addison’s
Endocrine
- Ectopic hormone secretion
o SIADH and ACTH by small cell tumours (low Na, high ADH, cushingoid)
o PTH by squamous cell (high Ca)
Neurological
- Eaton-lambert syndrome (proximal myopathy and decreased reflexes),
confusion, fits, cerebellar syndrome, neuropathy, polymyositis
Other
- clubbing
- Hypertrophic Pulmonary OA
- Dermatomyositis
- Acanthosis nigricans
- Thrombophlebitis migrans
EXAMINATION
General
- Cachexia, pallor
- Fever
- Gynecomastia (any kind), cushingoid features (small cell)
- Hoarse voice
Peripheries and Face
- Clubbing (non-small cell)
- HPOA (hypertrophic pulmonary osteoarthropathy) causing wrist pain
- Supraclavicular/axillary nodes (non-small cell)
- Horner’s syndrome, SVC compression
Chest
- May be none
- Inspection - dilated veins (SVC obstruction)
- Palpation - Bony pain
- Auscultation/Percussion – Consolidation, collapse, pleural effusion
Neuro
- Confusion (cortical degeneration)
- Peripheral/autonomic neuropathy
- Eaton Lambert’s syndrome (small cell)
Skin
- DIC, migrating thrombophlebitis
- Acanthosis nigricans
- Purpura
- Scleroderma
Signs of Metastases
- Bone tenderness
- Hepatomegaly
- Focal neuro signs/confusion
- Cerebellar syndrome
Differential dx for lung nodule on CXR
- Malignancy
- Abscesses
- Granuloma
- Carcinoid tumour
- Pulmonary hamartoma
- AV malformation
- Cyst
- Foreign body
- Skin tumour
IX for dx, staging, treatment of lung cancer,
INVESTIGATIONS for dx
- Cytology
o Sputum if central
o Pleural fluid if effusion (LIGHTs)
o CXR
Peripheral nodule (adenocarcinoma)
Hilar enlargement (small
cell)
Consolidation, collapse,
pleural effusion
Bony secondaries
- Bronchoscopy
Biopsy/fine needle Aspirate
Assess operability - Percutaneous FNA or video-assisted thoracoscopy biopsy
INVESTIGATIONS FOR STAGING - TNM
o FBC, Ca, LFT’s
o ACTH, ADH, Na
o CT
o PET
- Bone scan if suspect metastases
INVESTIGATIONS FOR TREATMENT
- Lung function tests
o If FEV1 > 1.5L indicates that patient could tolerate a pneumonectomy
o Patient that can climb three flights of stairs
o ECOG status
Management of small cell and non-small cell
Non-small Cell
- Excision if localized and no mets (1/3rd patients)
- Curative radiotherapy if resp reserve poor
- Chemo + radio for more advanced disease
(Stage IV)
Small Cell
- Immunotherapy plus…
- Chemotherapy with platinum-based drugs
e.g. cisplatin but invariably relapse
- Prophylactic cranial irradiation in patients
with complete responses
- Palliation
o Radiotherapy for bronchial
obstruction, SVC obstruction, haemoptysis, bone pain and cerebral mets
o Endobronchial therapy e.g. tracheal stenting, cryotherapy, brachytherapy
o Pleural drainage for symptomatic pleural effusions
o Drugs like analgesia, steroids, antiemetics, cough suppressants, bronchodilators, antidepressants
Differential dx for daytime sleepiness + risk factors
DIFFERENTIAL DIAGNOSIS OF DAYTIME SLEEPINESS
- Not enough sleep/poor sleep hygiene
- Poor adjustment to shift work
- Use of sedative/stimulant drugs
- Depression, with or without early morning
waking
- Idiopathic hypersomnolence (sleepiness despite plenty of sleep without snoring)
- Narcolepsy
MEDICAL CONDITIONS WHICH INCREASE RISK
- pregnancy
- heart failure
- renal disease
- lung disease (asthma, COPD, ILD etc)
- CVA
- acromegaly
- hypothyroidism
- PCOS
- T2DM
- Parkinson’s
Exam for OSA - cessation of breathing >10s + complications of untreated OSA
General
- BMI
- Acromegaly (big hands feet face-pit tumour)
Peripheries and Face
- Blood pressure
- Fundi for signs of HTN
- Signs of hypothyroidism
- Head/neck/mouth for signs of uvular enlargement/macroglossia/tonsillar hypertrophy.
- Neck circumference
Chest
- Respiratory usually normal
- Look for signs of pulmonary hypertension
- Signs of cor pulmonale
o Cyanosis, tachycardia, raised JVP with prominent a and v waves, RV heave, loud P2, pansystolic murmur
(tricuspid regurgitation),
hepatomegaly, oedema.
Neurological
- Causes of obstructive sleep apnoea
o Myasthenia gravis
o Muscular dystrophy
- Causes of central sleep apnoea
o Autonomic neuropathy
o Brain stem lesions
o Spinal cord disease
COMPLICATIONS
Pulmonary hypertension -> right ventricular dysfunction –> cor pulmonale –>type two respiratory failure
Risk of MVAs
Neuropsychiatric dysfunction
Cardio morbidity
T2DM and NA-FattyLD
OSA is also an independent risk factor for HTN
Ix, dx and treatment of OSA
INVESTIGATIONS
- Sleep study/polysomnography (measures oxygen sats, airflow at nose and mouth, ECG, chest wall movements) is diagnostic
- TFT’s (for hypothyroidism
- ECG to Assess RV dysfunction
- Epworth Sleepiness Scale
Dx
- > 5 apnoeic episodes per hour, over several hours, lasting > 10 seconds each
- Apnoea Hypopnoea Index (AHI) = number of episodes/number of hours slept
o Mild 5 – 15
o Moderate 16 – 30
o Severe > 30
TREATMENT
- Weight loss
- Avoid tranquilizers, sedatives
- Alcohol and smoking reduction
- Reverse underlying cause if possible- eg. Thyroid replacement, Surgical correction of upper airways
narrowing (polyps, macroglossia, tonsillectomy)
- Vigorously treat concomitant diseases
o Cardiac failure, hypertension, asthma - CPAP for moderate to severe OSA
o Modafinil if residual sleepiness - BiPAP for central sleep apnoea (stroke)
Sarcoidosis clinical presentation/ features (10)
Usually affects adults 20-40s, Northern
Europe, Blacks > whites. More frequently women.
Associated with HLA-DRB1 and DQD1 alleles
50% incidental Bilateral hilar lymphadenopathy on CXR
- acute presentation - E.nodosum, polyarthralgia, fever, & BHL – resolves
spontaneously
- Pulmonary disease (90% have)
o Bilateral hilar lymphadenopathy
o Pulmonary infiltrates or fibrosis
o Dry cough, progressive dyspnoea, reduced exercise tolerance, chest pain
o 10-20% sx progress w subsequent deterioration in lung function. - Extra-pulmonary manifestations (~30%)
o lymphadenopathy
o Abdo: hepatomegaly, splenomegaly
o Eye: uveitis, conjunctivitis,
keratoconjunctivitis sicca, glaucoma
o Enlarged lacrimal and parotid glands
o Terminal phalangeal bone cysts
o Skin: erythema nodosum (a), lupus pernio (c), subcutaneous nodules
o Heart: cardiomyopathy, arrhythmias
o hyperCa, renal stones
o Neuro: Bell’s palsy, optic neuritis, meningitis, Brown sequard & spinal syndromes, space-occupying lesion
Investigations for sarcoid
- staging on CXR (4)
Blood: Raised ESR, lymphopenia, raised LFT, raised serum ACE, raised Ca and Ig.
Urine: Raised Ca - macrophages make more vit D
Tuberculin skin test: Neg (60%)
CXR (stages)
- 1 – BHL
- 2 – BHL + peripheral pulmonary infiltrates
- 3 – peripheral pulmonary infiltrates alone
- 4 – Pulmonary fibrosis, bulla (honeycombing), pleural involvement
USS: may show nephrocalcinosis, or
hepatosplenomegaly
PulFT: N or reduced volumes, impaired gas transfer, restrictive pattern
Biopsy: non-caseating granulomata (diagnostic)
Bronchoalveolar lavage:
- Raised lymphocytes in active disease
- Neutrophils in pulmonary fibrosis
Bone x-rays: punched out lesions in terminal phalanges
CT/MRI: pulmonary disease severity or Dx neurosarcoidosis. Panda sign; enlarged parotids/lacrimal
glands. Lambda sign; R paratracheal + L hilar.
Ophthalmology assessment: if eye involvement
Management + monitoring for sarcoidoidosis
PROGNOSIS
60% thoracic sarcoidosis resolve over 2yrs.
20% respond to steroid Tx; in the rest, improvement unlikely despite Tx
MANAGEMENT
BHL alone don’t need Tx – most recover
Acute sarcoidosis: bed rest & NSAIDs
Indications for steroids;
- Parenchymal lung disease (Sx, static,progressive)
- Uveitis
- Hypercalcaemia
- Neuro, renal or cardiac involvement
Prednisone 20-40mg OD for 4-6 weeks then decrease dose over 1yr according to clinical status.
(Higher doses may be warranted in very severe
cases.)
Topical steroids: skin manifestations.
Other:
- If severe illness, IV methylpred
Differential dx for Bilateral hilar lymphadenopathy
granulomatous disease
*DDx for BHL
- sarcoidosis
- infection; TB, mycoplasma
- Malignancy: lymphoma, carcinoma, M/S
- Extrinsic allergic alveolitis
- Histiocytosis X
- DDx granulomatous disease
- Infections: TB, leprosy, syphilis, cat scratch fever,
- Autoimmune: PBC, granulomatous orchitis
- Vasculitis: GCA, polyarteritis nodosa, Takayasu’s arteritis
- Organic: silicosis, berylliosis
- Idiopathic: Crohn’s, Sarcoidosis, de Quervain’s
thyroiditis - Other: EAA, Histiocytosis X
Clinical manifestations of TB - what to look for - risk factors is renal disease, malignancy, HIV, T2DM, age extremes
Pulmonary:
silent or cough, sputum, malaise, weight loss, night
sweats, pleurisy, haemoptysis, pleural effusion, superimposed pulmonary infection
Milliary:
Haematogenous spread. Non-specific or
overwhelming signs. Nodular opacities on CXR.
Look for retinal TB.
Genitourinary:
Dysuria, freq, loin pain, haematuria, sterile pyruia
Bone:
Vertebral collapse and Pott’s vertebra
Skin (lupus vulgaris):
jelly-like nodules on face/neck
Meningitis:
Prodrome: fever, headache, V, abdo pain, drowsy,
meningism, delirium over 1-3wks. CND+S signs of CN palsies, papilloedmea
Dx by LP, TB PCR, look for immunosuppression elsewhere (i.e. HIV), MRI/CT. 30% mortality.
