RESP Flashcards
1
Q
Aspergillus Lung Disease Def.
A
Lung disease associated with Aspergillus lung infection
2
Q
Aspergillus Lung Disease Types & Presentations
A
Aspergilloma
- Fumigatus mycetoma ball in pre-existing lung cavity (post-TB, old infarct)
- Presents: Asymptomatic, haemoptysis
ABPA
- Colonisation of airways, common in asthmatics
-IgE & IgG immune response (proteolytic enzymes, mycotoxins, antibodies) leads to airway damage
- Presents: uncontrollable asthma, recurrent pneumonia with wheeze, cough, fever, malaise
Invase Aspergillosis
- Invasion into lung tissue & fungal dissemination, common in immunocompromised (neutropenia, steroid use, AIDS)
- Presents: Dyspnoea, Rapid Deterioration, Septic Picture
3
Q
Aspergillus Lung Disease Epidemiology
A
- Elderly & Immunocompromised
- Uncommon
4
Q
Aspergillus Lung Disease SIGNS
A
- Tracheal Deviation (if large)
- Dullness in lung
- Reduced breath sounds
- Wheeze in ABPA
- Cyanosis
5
Q
Aspergillus Lung Disease Investigations
A
ASPERGILLOMA
- CXR shows round mass with crescent of air around it
- CT/MRI if unclear
- Sputum cultures negative if there is no communication between cavity colonised by Aspergillus & Bronchial Tree
ABPA
- Skin test reactivity to Asp. antigens
- Bloods: Eosinophilia, increased IgE & IgE/IgG specific to A.fumigatus
- CXR shows transient patchy shadows, collapse, distended mucous-filled bronchi. If complicated then there will also be fibrosis in upper lobes & bronchiectasis
- Lung function tests show reversible airflow limitation (reduced lung vol/ gas transfer)
INVASIVE ASPERGILLOSIS
- Dx via cultures & histological examination
- Bronchoalveolar lavage fluid/ sputum used diagnostically
- Chest CT shows nodules surrounded by ground-glass appearance. (haemorrhage into tissue surrounding area of fungal invasion)
6
Q
Asthma Definition
A
Chronic inflammatory airway disease characterised by reversible airway obstruction, airway hyper-responsiveness and bronchial inflammation
7
Q
Asthma Risk Factors
A
Genetic: Family History, Atopy (T lymph. drive production of IgE on exposure to antibodies)
Environmental: House mites, pollen, pets, cigarette smoke, viral RTI, Aspergillus spores, occupational allergens
8
Q
Asthma Epidemiology
A
10% children, 5% adults with increasing prevalence
9
Q
Asthma presenting symptoms
A
- Episodic Hx
- Wheeze
- Breathlessness
- Cough (worse morning & night)
- important to ask about previous hospitalisations to gauge severity
- Precipitated by cold, virus, drugs (Beta-blockers, NSAIDs, exercise, emotions)
10
Q
Asthma Signs
A
-Tachypnoea
- use of accessory muscles
-prolong expiratory phase
-polyphonic wheeze
-hyper inflated chest
If severe: PEFR<50% predicted, pulse >110, RR >25, incomplete sentences
Life threatening: PEFR <33% predicted, silent chest, cyanosis, bradycardia, hypotension, confusion, coma
11
Q
Asthma Investigations (Acute & Chronic)
A
ACUTE
- Peak flow, pulse ox, ABG, CXR, FBC (increase WCC for infection), CRP, U&Es, Blood & Sputum
CHRONIC
- Peak flow monitor to se diurnal variation, pulmonary function test, bloods (eosinophilia, IgE, A.fumigatus), skin prick, spirometry
12
Q
Management of Acute Asthma
A
- ABCDE
- Resuscitate
- Monitor oxygen sats, ABG & PEFR
- High air flow Oxygen
- Salbutamol nebuliser (5mg 2-4hourly)
- Ipratropium Bromide (0.5mg QDS)
- Steroid therapy (100-200mg Iv hydrocortisone, followed by 40mg oral prednisone for 5-7 days
- If no improvement (PEFR<50% predicted) : IV Mg Sulphate infusion , IV salbutamol, IV aminophylline infusion
- Anaesthetic help if pt is getting exhausted (can tell this because PCO2 will be high as the patient is unable to hyperventilate and blow off CO2)
- Treat underlying cause e.g ABs if infective exacerbation
- Monitor electrolytes (bronchodilsators & aminophylline cause a drop in K+)
- Invasive ventilation may be needed in severe attacks
- Discharge when:
PEFR >75% predicted, diurnal variation <25%, inhaler technique checked, stable on discharge meds for 24h, pt. has own PEF meter, steroid & bronchodilator therapy - Arrange a follow up
13
Q
Management of chronic Asthma (5 Steps)
A
Step 1: inhaled SABA
Step 2: (if SABA used >1/day) add regular low-dose steroids (400mcg/day)
Step 3: Add LABA (Salmeterol). If inadequate, increase steroid dose to 800mcg/day. If no response to LABA, stop it and just use steroids
Step 4: Increase steroid dose (2000mcg/day). Add 4th drug (leyukotrine antagonist, slow-release theophylline/ B2 agonist tablet)
Step 5: Add regular oral steroids and maintain at high-dose, refer to specialist
Advice: teach technique, explain importance of PEFR monitoring, avoid provoking factors
14
Q
Complications of Asthma
A
- Growth retardation,
- Chest wall deformity (pigeon chest)
- Recurrent infections
- Pneumothorax
- Respiratory failure
- Death
15
Q
Asthma prognosis
A
Many children improve with age, but adult-onset asthma is usually chronic
16
Q
Define Bronchiecstasis
A
Lung airway disease characterised by chronic bronchial dilation, impaired mucociliary clearance and frequent bacterial infections
17
Q
Aetiology/ Risk Factors of bronchiectasis
A
Chronic lung inflammation leads to fibrosis & permanent dilation of the bronchi. Leads to pooling of mucus, predisposing to further infection, damage & fibrosis of bronchial walls
Causes:
- 50% idiopathic
- Post-infectious (pneumonia, whooping cough, TB)
- Host-defence defects (Kartagener’s syndrome, CF)
- Obstruction of bronchi (e.g. foreign body, enlarged lymph nodes)
- GORD
- Inflammatory disorders (Rheumatoid arthritis)
18
Q
Epidemiology of Bronchiecstasis
A
- mostly arises in childhood
- incidence has decreased with the use of antibiotics
- 1/1000 per year
19
Q
Presenting symptoms of bronchiecstasis
A
- Productive cough with purulent sputum or haemoptysis
- Breathlessness
- Chest pain
- Malaise
- Fever
- Weight loss
- Symptoms usually begin after an acute respiratory illness
20
Q
Signs of Bronchiecstasis on physical examination
A
- Clubbing
- Coarse crepitations at lung bases which shift with coughing
- Wheeze
21
Q
Investigations for Bronchiecstasis
A
- High-resolution CT is the GOLD STANDARD . Shows dilated bronchi with thickened walls
- Sputum ( culture & sensitivity. Pseudomonas aeruginosa = most common organism)
- CXR shows dilated bronchi (tramline shadows), fibrosis, atelectasis, pneumonic consolidations, may be normal though
- Bronchography is rarely used
22
Q
Management for Bronchiecstasis
A
- Treat acute exacerbations with 2 IV antibiotics, which cover Pseudonomas aeruginosa
- Prophylactic ABs in patients with frequent exacerbations (>3/year)
- Inhaled corticosteroids (e.g. flucticasone) - reduces inflammation and vol of sputum but doesn’t affect the frequency of exacerbations or lung function
- Maintain hydration
- Flu vaccination
- Phsyiotherapy (mucus clearance to reduce acute exacerbations & aid recovery)
- Bronchial artery embolisation (if life-threatening haemoptysis due to bronchiectasis)
- Surgical (localised resection, lung or heart-lung transplantation)
23
Q
Complications of Bronchiecstasis
A
- Life threatening haemoptysis
- Persistent infections
- Empyema
- Respiratory failure
- Cor pumonale
- Multi-organ abscesses
24
Q
Prognosis of patients with Bronchiecstasis
A
Most patients continue to have symptoms after 10 years
25
Define COPD
Chronic, progressive lung disorder characterised by airflow obstruction, with the following:
- Chronic bronchitis (cough&sputum on most days >3months/year over 2 consecutive years)
Narrowing of airways resulting in bronchiolitis, bronchial mucosal oedema, mucous hyper secretion, squamous metaplasia
- Emphysema (pathological diagnosis of permanent destructive enlargement of air spaces distal to the terminal bronchioles)
Destruction and enlargement of alveoli leads to loss of elasticity that keeps small airways open in expiration. Progressively larger spaces develop called bullae (diameter >1cm)
26
Aetiology/ Risk Factors of COPD
- bronchial & alveolar damage caused by environmental toxins (cigarette smoke)
- Rarely caused by alpha1-antitrypsin deficiency
(consider this in non-smoking, young patients)
27
Epidemiology of COPD
- Common (8% prevalence)
- Presents in middle age or later
- More common in males (may change bc smoking changes)
28
Presenting symptoms of COPD
- Chronic cough
- Sputum production
- Breathlessness
- Wheeze
- Reduced exercise tolerance
29
Signs of COPD on physical examination
```
Inspection:
- respiratory distress
- use of accessory muscles
- barrel-shaped over-inflated chest
- decreased cricosternal distances
- cyanosis
Percussion:
- hyper-resonant chest
- loss of liver and cardiac dullness
Auscultation
- quiet breath sounds
- prolonged expiration
- wheeze
- rhonchi - rattling, continuous and low pitched breath sounds that sound a bit like snoring. Often caused by secretion in larger airways or obstructions
- Sometimes crepitations
Signs of CO2 retention:
- bounding pulse
- warm peripheries
- asterixis
- later stages: RHF (cor pumonale) , right ventricular heave, raised JVP, ankle oedema
```
30
Investigations for COPD
Spirometry & Pulmonary function tests:
- obstructive picture
- reduced PEFR, FEV1/FVC
- increased lung volumes
- decreased CO gas transfer coefficient
CXR:
- may appear normal
- hyperinflation (>6 anterior ribs, flattened diaphragm)
- reduced peripheral lung markings
- elongated cardiac silhouette
Bloods:
- FBC- increased Hb & haematocrit due to secondary polycythaemia
-ABG- may show hypoxia, normal/ raised PCO2
- ECG & Echocardiogram - check for cor pulmonale
- Sputum & Blood cultures: useful in acute infective exacerbations
- Alpha1 antitrypsin levels- useful in young patients who have never smoked
31
Management for COPD
- Stop smoking
- Bronchodilators :
SABA (salbutamol), Anticholinergics (ipratropium bromide), LABA (if more than 2 exacerbations per year)
- Steroids ( inhaled beclamethasone considered in patients with FEV1<50% predicted OR >2 exacerbations per year) Avoid regular oral steroids
- Pulmonary rehab
- Oxygen therapy (only if stopped smoking, indicated if PaO2 <7.3kPa on air during a period of clinical stability
PaO2: 7.3-8kPa and signs on secondary polycythaemia, nocturnal hyperaemia, peripheral oedema or pulmonary hypertension
32
Treatment of acute exacerbations of COPD
- 24% O2 via venturi mask
- increase slowly if no hypercapnia and still hypoxic (do an ABG)
- corticosteroids
- empirical ABs if infection
- respiratory physiotherapy to clear sputum
- non invasive ventilation if severe
33
Complications of COPD
- Acute respiratory failure
- Infections
- Pulmonary hypertension
- RHF
- Pneumothorax
- Secondary polycythaemia
Give pneumococcal & influenza vaccination to prevent infective exacerbations
34
Prognosis of patients with COPD
- high morbidity
- 3-year survival of 90% if <60 yrs, FEV1>50% predicted
- 3-year survival of 75% if >90yrs, FEV1: 40-49% predicted
35
```
Hypersensitivity Pneumonia
(Extrinsic Allergic Alveolitis) definition
```
Interstitial inflammatory disease of the distal gas-exchanging parts of the lung caused by inhalation of organic dusts.
36
Aetiology/ Risk Factors for hypersensitivity pneumonitis
- inhalation of antigenic dusts induce a hypersensitivity response in susceptible individuals
- antigenic dusts include microbes & animal proteins
e. g. Farmer's lung (mouldy hay with thermophilic actinomycetes)
- Pigeon Fancier's lung - blood on bird feathers and excreta
- Maltworker's Lung (barley/ malting containing Aspergillus clavatus
37
Epidemiology of hypersensitivity pneumonitis
- uncommon
- 2% occupational lung disease
- 50% reported cases affect farm workers
- geographical variation
38
Presenting symptoms hypersensitivity pneumonitis (Acute vs Chronic)
```
ACUTE:
- 4-12hours after exposure, involving reversible episodes of:
- dry cough
- dyspnoea
- malaise
-fever
-myalgia
-wheeze and productive cough if repeated high-level exposure
CHRONIC:
- slowly increasing breathlessness
- decreased exercise tolerance
- weight loss
- chronic exposure may be low-level so no previous acute episode
```
Important to ask a full occupational Hx and enquire about hobbies and pets
39
Signs of hypersensitivity pneumonitis (acute vs chronic)
```
ACUTE:
- rapid shallow breathing
- pyrexia
- inspiratory crepitations
CHRONIC:
- fine inspiratory crepitations
- clubbing (rare)
```
40
Investigations for hypersensitivity pneumonitis
```
Bloods:
- FBC (neutrophilic, lymphopenia)
- ABG (reduced PO2 & PCO2)
Serology:
- Test for IgG to fungal or avian antigens
CXR:
- normal in acute episodes
- fibrosis may be seen in chronic cases
High Resolution CT-Thorax
- detects early changes
- patchy 'ground glass' shadowing and nodules
Pulmonary Function Tests:
- Restrictive defect (low FEV1, low FVC)
- Preserved or increased FEV1/ FVC ratio
- Reduced total lung capacity
Bronchoalveolar Lavage:
- increased cellularity
- lung biopsy
```
41
Definition of Idiopathic Pulmonary Fibrosis
Inflammatory condition of the lung resulting in fibrosis of the alveoli and interstitial. Previously known as cryptogenic fibrosing alveolitis
42
Aetiology/ Risk Factors Idiopathic Pulmonary Fibrosis
- occurs in genetically predisposed individuals
- recurrent injury to alveolar epithelial cells results in secretion of cytokines and growth factors
- Leads to fibroblast activation, recruitment, proliferation, differentiations into myofirboblasts and increased collagen synthesis and deposition
- Certain drugs can reproduce effects (MTX, amiodarone)
43
Histological patterns of Idiopathic Pulmonary Fibrosis
Interstitial pneumonia
44
Risk Factors Idiopathic Pulmonary Fibrosis
Smoking
Occupational Exposure to metal or wood
Chronic microaspiration
Animal and vegetable dusts
45
Summarise epidemiology of idiopathic pulmonary fibrosis
- Rare
- 6/100,000
- more common in MALES
46
Presenting symptoms Idiopathic pulmonary fibrosis
- gradual-onset, progressive dyspnoea on exertion
- dry irritating cough
- no wheeze
- symptoms may be preceded by a viral-type illness
- fatigue and weight loss are common
Important to take a full drug and occupational history
47
Signs of idiopathic pulmonary fibrosis on physical examination
- clubbing (50%)
- bibasal fine late inspiratory crackles
- signs of RHF in advanced stages
48
Investigations for Idiopathic Pulmonary Fibrosis
Lung Biopsy:
GOLD STANDARD
Bloods:
- ABG: normal in early disease, PO2 decreases with exercise, normal PCO2 which rises in late stage disease
- ANA and Rheumatoid Factor (1/3 all patients positive for either of these)
CXR:
- usually normal
- early disease may show ground glass shadowing
- later stages: reticulonodular shadowing, signs of cor pulmonale and eventually honeycombing
HIGH RES CT:
- more sensitive for early disease
Pulmonary function tests:
- restrictive features
- decreased lung vol, lung compliance, total lung capacity
Bronchoalveolar Lavage:
- exclude infections and malignancy
Echocardiography:
- check for pulmonary hypertension
49
Define Obstructive Sleep Apnoea
Disease characterised by recurrent prolapse of pharyngeal airway and apnoea (cessation of airflow >10seconds) during sleep, followed by arousal from sleep.
50
Aetiology/ Risk Factors Obstructive Sleep Apnoea
- Narrowing of upper airways because of collapse of soft tissues of pharynx
- Decreased tone of pharyngeal dilators during sleep
- Associated with: weight gain, smoking, alcohol, sedative use, enlarged tonsils & adenoids in children, macroglossia, marfans, craniofacial abnormalities
51
Epidemiology of Obstructive Sleep Apnoea
- common
- 5-20% men >35yrs
- 2-5% women >35yrs
- prevalence increases with age
52
Presenting symptoms of obstructive sleep apnoea
- excessive daytime sleepiness
- unrefreshing / restless sleep
- morning headaches
- difficulty concentration
- irritability and mood changes
- partner reporting snoring, nocturnal apnoea episodes or nocturnal choking
53
Signs of obstructive sleep apnoea on physical examination
- large tongue
- enlarged tonsils
- long/ thick uvula
- retrognathia
- neck circumference (>42cm in males, >40cm in females)
- obesity
- HTN
54
Investigations for Obstructive Sleep Apnoea
- Sleep study (monitor airflow, respiratory effort, pulse oximetry & HR)
- Bloods (TFTs, ABG)
55
Pneumoconiosis definition (and 3 different types)
Fibrosing interstitial lung disease caused by chronic inhalation of mineral dusts
Simple: coalworker's pneumoconiosis or silicosis
Complicated: pneumoconiosis results in loss of lung function
Asbestosis: pneumoconiosis in which different diffuse parenchymal lung fibrosis occurs as a result of prolonged exposure to asbestos
56
Aetiology/ Risk Factors of Pneumoconiosis
```
Inhalation of particles of:
- coal dusts
- silica
- asbestos
Risk Factors:
- occupational exposure
- risk depends on extent of exposure and particle type
- Individual susceptibility
- Cofactors such as smoking & TB also contribute
```
57
Epidemiology Pneumoconiosis
Increasing incidence in developing countries
| Disability and mortality from asbestosis will continue to increase for the next 20-30yrs
58
Presenting symptoms pneumoconiosis
Occupational History is very important
Asymptomatic: picked up on routine CXR
Symptomatic:
- insidious onset SOB
- dry cough
- Melanoptysis (coal worker's pneumoconiosis)
- Pleuritic chest pain (acute asbestos pleurisy)
59
Signs of Pneumoconiosis on physical examination
- Expiration may be normal
- Coalworkers pneum. & silicosis: decreased breath sounds
- Asbestosis: end-inspiratory crepitations, clubbing
- Signs of pleural effusion or RHF (cor-pulmonale)
60
Investigations for pneumoconiosis
CXR:
Simple shows micro nodular mottling
Complicated: shows nodular opacities in upper lobes, micro nodular shadowing, eggshell calcification of hilar lymph nodes (in silicosis), bilateral lower zone reticulonodular shadowing and pleural plaques (in asbestosis)
CT scan: fibrotic changes can be visualised early
Bronchoscopy: allows visualisation and bronchoalveolar lavage
Lung Function Tests: restrictive pattern
61
Define Pneumonia
Infection of distal lung parenchyma
- CAP
- HAP
- Aspiration pneumonia
- Pneumonia in the immunocompromised
- Typical
- Atypical
62
Aetiology/ Risk factors of pneumonia (HAP & CAP)
CAP:
- 70% Streptococcus pneumoniae
- Haemophilus influenza
- Moraxella Catarrhalis (COPD patients)
- Chlamydia pneumonia
- Mycoplasma pneumonia
- Legionella
- Staphylococcus aureus
- Coxiella Burnetii
- TB
HAP:
- Gram negative enterobacteria (Pseudomonas, Klebsiella)
- Anaerobes (aspiration pneumonia)
Risk Factors:
- Age
- Smoking
- Alcohol
- Pre-existing lung disease (COPD)
- Immunodeficiency
- Contact with pneumonia patients
63
Epidemiology of pneumonia
5-11/ 1000
| CAP responsible >60,000 deaths per year in the UK
64
Presenting symptoms of pneumonia (and specifically to atypical)
- Fever
- Rigors
- Sweating
- Malaise
- Cough
- Sputum
- Breathlessness
- Pleuritic chest pain
- Confusion
ATYPICAL
- headache
- myalgia
- diarrhoea/ abdo pain
- dry cough
65
Recognise signs of pneumonia on physical examination
- pyrexia
- respiratory distress
- tachypnoea
- tachycardia
- hypotension
- cyanosis
- decreased chest expansion
- dull to percuss over affected area
- increased tactile vocal fremitus over affected area
- bronchial breathing over affected area
- coarse crepitations on affected sides
Chronic suppurative lung disease (empyema, abscess)--> clubbing
66
Investigations for pneumonia
Bloods:
FBC- raised WCC, E&Es, LFTs, Blood cultures, ABG, Blood film (mycoplasma causes red cell agglutination)
CXR:
Lobar or patchy shadowing, pleural effusion, (klebsiella affects upper lobes)
Sputum/ Pleural Fluid- MC&S
Urine- pneumococcus and legionella antigens
Atypical viral serology
Bronchoscopy and bronchoalveolar lavage- if pneumocystis carinii pneumonia is suspected, or if pneumonia fails to resolve
67
Management plan for pneumonia
- Assess severity with British Thoracic Society Guidelines
- Start empirical antibiotics: Oral amoxicillin if 0 markers
Oral/ IV Amoxicillin & Erythromycin if 1 marker
IV Cefuroximine/ Cefotaxime/ Co-amoxiclav +Erythromycin (>1 marker)
Add metronidazole if aspiration, lung abscess of empyema
- Use AB appropriate to sensitivity
- Supportive treatment : O2, IV fluids, CPAP BiPAP or ITU care for respiratory failure, and surgical drainage if lung abscesses and empyema
- Discharge planning
if two or more features of clinical instability are present (e.g. temp, tachycardia, tachypnoea, hypotension, low O2 sats) there is a high risk of re-admission and mortality
68
Prevention of Pneumonia
- pneumococcal vaccine
- haemophilus influenza type B vaccine
(only for high risk groups)
69
Complications of Pneumonia
- Pleural effusion
- Empyema
- localised suppuration (e.g. abscess, symptoms are: swinging fever, persistent pneumonia, copious/ foul-smelling sputum)
- Septic shock
- ARDS
- Acute renal failure
- Extra complications of mycoplasma pneumonia :
erythema multiforme
myocarditis
haemolytic anaemia
meningoencephalitis
transverse myelitis
Guillain-barre syndrome
70
Prognosis for patients with pneumonia
- most resolve with treatment within 1-3 weeks
- severe pneumonia has high mortality
- CURB-65 score assesses severity of pneumonia:
Confusion <8 AMTS
Urea >7 mmol/L
RR >30/min
BP: systolic <90mmHg or diastolic <60mmHg
Age >65yrs
71
Define Pneumothorax
Air in the pleural space
72
Aetiology/ Risk Factors of pneumothorax
Spontaneous:
- occurs in ppl with typically normal lungs
- typically tall, thin males
- rupture of sub pleural bleb
Secondary:
- in patients with pre-existing lung disease (COPD, asthma, TB)
Traumatic:
- penetrating injury to the chest
- often iatrogenic (i.e. during jugular venous cannulation)
Risk Factors:
- Collagen disorders (Marfans, Ehlers-Danlos)
73
Epidemiology of pneumothorax
- annual incidence: 9/100,000
- mainly 20-40yr olds
- 4x more common in MALES
74
Presenting symptoms of pneumothorax
- may be asymptomatic
- sudden onset breathlessness
- pleuritic chest pain
- distress with rapid shallow breathing (if tension pneumothorax)
75
Signs of pneumothorax on physical examination (and for tension pneumothorax)
-none if small
- signs of respiratory distress
- reduced expansion
- hyper-resonance to percussion
- reduced breath sounds
TENSION:
- severe respiratory distress
- tachycardia
- hypotension
- cyanosis
- distended neck veins
- tracheal deviation away from pneumothorax
76
Investigations for pneumothorax
CXR:
- dark area of film with no vascular markings
- fluid level may be seen if there is bleeding
ABG:
- check for hyperaemia
77
Management plan for pneumothorax
• Tension pneumothorax (emergency):
o Maximum O2, insert large-bore needle into second intercostal space, midclavicular line, on side of pneumothorax to relieve pressure, insert chest drain soon after
• Small pneumothorax (<2 cm lung-pleural margin):
o If there is no underlying lung disease, pleural fluid or clinical compromise, reassure, analgesia if required
• Moderate pneumothorax (>2 cm lung-pleural margin):
o Aspiration using large-bore cannula or catheter with three-way tap: inserted into the second intercostal space in the midclavicular line. Up to 2.5 L of air can be aspirated (stop if patient repeatedly coughs or resistance is felt). Follow-up CXR should be performed just after, 2 h and 2 weeks later. Advised to avoid diving
o Chest drain with water seal: if aspiration fails or if there is fluid in the pleural cavity or after decompression of a tension pneumothorax. It is inserted into the fourth to sixth intercostal space in midaxillary line
• Recurrent pneumothoraces: chemical pleurodesis (visceral and parietal pleura fusion with tetracycline or talc). Surgical pleurectomy
• Advice: Avoiding air travel until follow-up CXR confirms resolution of pneumothorax. Avoid diving unless bilateral surgical pleurectomy
78
Complications of pneumothorax
- recurrent pneumothoraces
| - bronchopleural fistula
79
Summarise the prognosis for patients with pneumothorax
- after having one , 20% patients will have another and frequency increases thereafter
80
Define Pulmonary Embolism
Occlusion of pulmonary vessels, most commonly by a thrombus that has travelled to the pulmonary vascular system from another site
81
Aetiology / Risk Factors of Pulmonary Embolism
Thrombus :
- 95% from DVT
- Rarely arises in right atrium (other than AF patients)
Other:
- amniotic fluid, air, fat, tumour, mycotic
Risk Factors:
- surgical patients
- immobility
- obesity
- OCP
- Heart Failure
- Malignancy
82
Epidemiology of PE
- relatively common
| - occur in 10-20% of patients with confirmed proximal DVT
83
Presenting symptoms of PE
- depends on site and size of embolus
- Small: asymptomatic
- Moderate: sudden onset SOB, cough, haemoptysis, pleuritic chest pain
- Large: as above and severe central pleuritic chest pain, shock, collapse, acute RHF, sudden death
- Multiple recurrent: symptoms of pulmonary HTN
84
Signs of PE on physical examination
Small: no clinical signs, maybe tachycardia and tachypnoea
Moderate: tachypnoea, tachycardia, pleural rub, low O2 sats despite supplementation
Large: shock, cyanosis, right hear strain (raised JVP, left parasternal heave, accentuated S2 sound)
Multiple recurrent: signs of pulmonary HTN, RHF signs
85
Investigations for a PE
- Using Wells score
- <4 Wells = low probability, use D-dimer
- >4 Wells, image with CTPA plus additional Ix
- Bloods: ABG, thrombophilia screen
- ECG: may be normal, or tachycardia, right axis dev., RBBB, S1Q3T3 pattern
- CXR: normal, but useful to exclude other Dx
- Spiral CT Angiogram (1st line) : poor sensitivity for small emboli, very sensitive for medium to large emboli
- VQ scan: mismatch indicates an area of infarcted lung
- Pulmonary Angiography: invasive & rarely necessary
- Doppler US of lower limb: assesses venous thromboembolism
- Echocardiography: may show right heart strain
86
Management plan for PE
Primary prevention:
compression stockings, heparin prophylaxis if at risk, good mobilisation & adequate hydration
Haemodynamically stable:
oxygen, anticoagulation with heparin/ LMWH, switch to oral warfarin for at least 3 months (maintain INR 2-3), analgesia
```
Haemodynamically unstable (massive PE):
resuscitate, oxygen, IV fluids, thrombolysis with tPA if cardiac arrest is imminent
```
Surgical/ Radiological:
embolectomy, IVC filters (for recurrent PEs when anticoagulant is contraindicated/ not working)
87
Complications of PE
- death
- pulmonary infarction
- pulmonary HTN
- RHF
88
Prognosis for patients with PE
- 30% mortality in untreated
- 8% mortality with treatment
- Increased risk thromboembolic disease
89
Define Tuberculosis (Primary/ Miliary/ Post-primary)
Granulomatous disease caused by Mycobacterium TB
Primary: initial infection may be pulmonary or (rarely) gastrointestinal
Miliary: haematogenous dissemination of TB
Post-primary: caused by reinfection or reactivation
90
Aetiology of TB/ Risk Factors
Mycobacterium tuberculosis is an intracellular organism that survives phagocytosis
RF: immunocompromised, infection with TB bacterium
91
Epidemiology of TB
Annual mortality= 3million
Annual UK incidence= 6000
Asian immigrants are highest risk group in UK
92
Symptoms & Signs of TB
Primary: asymptomatic, fever, malaise, cough, wheeze, erythema nodosum, phlyctenular conjunctivitis
Miliary: fever, weight loss, meningitis, yellow caseous tubercles spread to other organs
Post-primary TB: fever/night sweats, malaise, breathlessness, cough, sputum, haemoptysis, pleuritic chest pain, signs of pleural effusion, collapse, consolidation, fibrosis
Non-pulmonary TB: mainly in the immunocompromised
Lymph Nodes: suppuration of cervical lymph nodes leading to abscesses/ sinuses
CNS: meningitis, tuberculoma
Skin: lupus vulgaris (jellylike reddish-brown glistening plaques
Heart: pericardial effusion, constructive pericarditis
GI: subacute obstruction, change in bowel habit, weight loss, peritonitis, ascites
Genitourinary: UTI symptoms, renal failure, epididymitis, endometrial/ tubal involvement, infertility
Adrenal insufficiency
Bone/ Joint: osteomyelitis, arthritis, vertebral collapse (pott's disease), spinal cord, compression from an abscess
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Investigations for TB
Sputum/Pleural fluid/ bronchial washings - MC&S
Tuberculin tests: positive is pt has previous exposure to M.tuberculosis/ BCG
Mantoux test: purified protein derivative (PPD) injected intradermally, erythema occurs after 72hours
Heaf Test: drop of PPD on forearm, fire spring-loaded needle gun, check after 3-7 days, graded according to papule size & vesiculation
Interferon Gamma tests: useful in latent TB, exposure of host T cells to TB antigens leads to release of interferon
CXR:
Primary Infections: peripheral consolidation, hilar lymphadenopathy
Miliary Infection: fine shadowing
Post-primary: upper lobe shadowing, streaky fibrosis & cavitation, calcification, pleural effusion, hilar lymphadenopathy
HIV Testing
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Management of TB
- Antimicrobial therapy: combined to prevent resistance.
- Directly observed therapy (DOT) may be necessary. Treat for 6 months in pulmonary, 12months for bone or brain.
- Side effects:
Rifampicin: orange body fluids, enzyme inducing
Isoniazid: pyridoxine deficiency, peripheral neuropathy
Ethambutol: optic neuropathy
Pyrazinamide: increased rate/ arthralgia, hepatotoxicity
Streptomycin: only if highly resistant
Advice: explain SEs and consider steroids for pericardial, cerebral or bone involvement
Public Health: notifiable disease, isolate if respiratory until 2 weeks treatment
Contact tracing
Prevent: BCG vaccine (60-80% efficacy. live attenuate strain derived from mycobacterium Bovis)
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Complications of TB
Primary TB: lobar collapse (middle) and bronchiectasis (Brock's syndrome) , pleural effusion, pneumonic spread, military disease disseminated in lung/ body
Post-primary TB: pleural effusion, empyema, aspergilloma, adenocarcinoma, laryngeal disease, swelling of bronchial lymphatics & airflow obstruction, haemoptysis, distant spread
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Prognosis of TB
Excellent if pulmonary TB & treated. Overall mortality 8% is extra pulmonary TB, relapse because of non-adherence, resistance, cavitation, empyema, latency
